Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells
Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and...
Ausführliche Beschreibung
Autor*in: |
Gu, Huijie [verfasserIn] |
---|
Format: |
E-Artikel |
---|---|
Sprache: |
Englisch |
Erschienen: |
2015transfer abstract |
---|
Schlagwörter: |
---|
Umfang: |
10 |
---|
Übergeordnetes Werk: |
Enthalten in: 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS - 2012, ECR, Orlando, Fla |
---|---|
Übergeordnetes Werk: |
volume:339 ; year:2015 ; number:1 ; day:15 ; month:11 ; pages:112-121 ; extent:10 |
Links: |
---|
DOI / URN: |
10.1016/j.yexcr.2015.08.005 |
---|
Katalog-ID: |
ELV023966513 |
---|
LEADER | 01000caa a22002652 4500 | ||
---|---|---|---|
001 | ELV023966513 | ||
003 | DE-627 | ||
005 | 20230625141948.0 | ||
007 | cr uuu---uuuuu | ||
008 | 180603s2015 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1016/j.yexcr.2015.08.005 |2 doi | |
028 | 5 | 2 | |a GBVA2015021000009.pica |
035 | |a (DE-627)ELV023966513 | ||
035 | |a (ELSEVIER)S0014-4827(15)30067-7 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
082 | 0 | |a 570 | |
082 | 0 | 4 | |a 570 |q DE-600 |
082 | 0 | 4 | |a 610 |q VZ |
082 | 0 | 4 | |a 610 |q VZ |
084 | |a 44.44 |2 bkl | ||
100 | 1 | |a Gu, Huijie |e verfasserin |4 aut | |
245 | 1 | 0 | |a Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
264 | 1 | |c 2015transfer abstract | |
300 | |a 10 | ||
336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
337 | |a nicht spezifiziert |b z |2 rdamedia | ||
338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
520 | |a Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. | ||
520 | |a Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. | ||
650 | 7 | |a JNK |2 Elsevier | |
650 | 7 | |a Human adipose-derived mesenchymal stem cells |2 Elsevier | |
650 | 7 | |a Osteogenesis |2 Elsevier | |
650 | 7 | |a Adipogenesis |2 Elsevier | |
700 | 1 | |a Huang, Zhongyue |4 oth | |
700 | 1 | |a Yin, Xiaofan |4 oth | |
700 | 1 | |a Zhang, Jieping |4 oth | |
700 | 1 | |a Gong, Lunli |4 oth | |
700 | 1 | |a Chen, Jiong |4 oth | |
700 | 1 | |a Rong, Ke |4 oth | |
700 | 1 | |a Xu, Jun |4 oth | |
700 | 1 | |a Lu, Lixia |4 oth | |
700 | 1 | |a Cui, Lei |4 oth | |
773 | 0 | 8 | |i Enthalten in |n Academic Press |t 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |d 2012 |d ECR |g Orlando, Fla |w (DE-627)ELV011050691 |
773 | 1 | 8 | |g volume:339 |g year:2015 |g number:1 |g day:15 |g month:11 |g pages:112-121 |g extent:10 |
856 | 4 | 0 | |u https://doi.org/10.1016/j.yexcr.2015.08.005 |3 Volltext |
912 | |a GBV_USEFLAG_U | ||
912 | |a GBV_ELV | ||
912 | |a SYSFLAG_U | ||
912 | |a SSG-OLC-PHA | ||
912 | |a GBV_ILN_70 | ||
936 | b | k | |a 44.44 |j Parasitologie |x Medizin |q VZ |
951 | |a AR | ||
952 | |d 339 |j 2015 |e 1 |b 15 |c 1115 |h 112-121 |g 10 | ||
953 | |2 045F |a 570 |
author_variant |
h g hg |
---|---|
matchkey_str |
guhuijiehuangzhongyueyinxiaofanzhangjiep:2015----:oefjntriaknsitesegncnaioeidfeetainfuaaio |
hierarchy_sort_str |
2015transfer abstract |
bklnumber |
44.44 |
publishDate |
2015 |
allfields |
10.1016/j.yexcr.2015.08.005 doi GBVA2015021000009.pica (DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Gu, Huijie verfasserin aut Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier Huang, Zhongyue oth Yin, Xiaofan oth Zhang, Jieping oth Gong, Lunli oth Chen, Jiong oth Rong, Ke oth Xu, Jun oth Lu, Lixia oth Cui, Lei oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 https://doi.org/10.1016/j.yexcr.2015.08.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 339 2015 1 15 1115 112-121 10 045F 570 |
spelling |
10.1016/j.yexcr.2015.08.005 doi GBVA2015021000009.pica (DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Gu, Huijie verfasserin aut Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier Huang, Zhongyue oth Yin, Xiaofan oth Zhang, Jieping oth Gong, Lunli oth Chen, Jiong oth Rong, Ke oth Xu, Jun oth Lu, Lixia oth Cui, Lei oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 https://doi.org/10.1016/j.yexcr.2015.08.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 339 2015 1 15 1115 112-121 10 045F 570 |
allfields_unstemmed |
10.1016/j.yexcr.2015.08.005 doi GBVA2015021000009.pica (DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Gu, Huijie verfasserin aut Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier Huang, Zhongyue oth Yin, Xiaofan oth Zhang, Jieping oth Gong, Lunli oth Chen, Jiong oth Rong, Ke oth Xu, Jun oth Lu, Lixia oth Cui, Lei oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 https://doi.org/10.1016/j.yexcr.2015.08.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 339 2015 1 15 1115 112-121 10 045F 570 |
allfieldsGer |
10.1016/j.yexcr.2015.08.005 doi GBVA2015021000009.pica (DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Gu, Huijie verfasserin aut Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier Huang, Zhongyue oth Yin, Xiaofan oth Zhang, Jieping oth Gong, Lunli oth Chen, Jiong oth Rong, Ke oth Xu, Jun oth Lu, Lixia oth Cui, Lei oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 https://doi.org/10.1016/j.yexcr.2015.08.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 339 2015 1 15 1115 112-121 10 045F 570 |
allfieldsSound |
10.1016/j.yexcr.2015.08.005 doi GBVA2015021000009.pica (DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 DE-627 ger DE-627 rakwb eng 570 570 DE-600 610 VZ 610 VZ 44.44 bkl Gu, Huijie verfasserin aut Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells 2015transfer abstract 10 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier Huang, Zhongyue oth Yin, Xiaofan oth Zhang, Jieping oth Gong, Lunli oth Chen, Jiong oth Rong, Ke oth Xu, Jun oth Lu, Lixia oth Cui, Lei oth Enthalten in Academic Press 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS 2012 ECR Orlando, Fla (DE-627)ELV011050691 volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 https://doi.org/10.1016/j.yexcr.2015.08.005 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 44.44 Parasitologie Medizin VZ AR 339 2015 1 15 1115 112-121 10 045F 570 |
language |
English |
source |
Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 |
sourceStr |
Enthalten in 72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS Orlando, Fla volume:339 year:2015 number:1 day:15 month:11 pages:112-121 extent:10 |
format_phy_str_mv |
Article |
bklname |
Parasitologie |
institution |
findex.gbv.de |
topic_facet |
JNK Human adipose-derived mesenchymal stem cells Osteogenesis Adipogenesis |
dewey-raw |
570 |
isfreeaccess_bool |
false |
container_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
authorswithroles_txt_mv |
Gu, Huijie @@aut@@ Huang, Zhongyue @@oth@@ Yin, Xiaofan @@oth@@ Zhang, Jieping @@oth@@ Gong, Lunli @@oth@@ Chen, Jiong @@oth@@ Rong, Ke @@oth@@ Xu, Jun @@oth@@ Lu, Lixia @@oth@@ Cui, Lei @@oth@@ |
publishDateDaySort_date |
2015-01-15T00:00:00Z |
hierarchy_top_id |
ELV011050691 |
dewey-sort |
3570 |
id |
ELV023966513 |
language_de |
englisch |
fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV023966513</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625141948.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.yexcr.2015.08.005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015021000009.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV023966513</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4827(15)30067-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.44</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Gu, Huijie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">10</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">JNK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Human adipose-derived mesenchymal stem cells</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Osteogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Adipogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Zhongyue</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yin, Xiaofan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Jieping</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gong, Lunli</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Jiong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rong, Ke</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Jun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lu, Lixia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cui, Lei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="t">72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS</subfield><subfield code="d">2012</subfield><subfield code="d">ECR</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV011050691</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:339</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:1</subfield><subfield code="g">day:15</subfield><subfield code="g">month:11</subfield><subfield code="g">pages:112-121</subfield><subfield code="g">extent:10</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.yexcr.2015.08.005</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.44</subfield><subfield code="j">Parasitologie</subfield><subfield code="x">Medizin</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">339</subfield><subfield code="j">2015</subfield><subfield code="e">1</subfield><subfield code="b">15</subfield><subfield code="c">1115</subfield><subfield code="h">112-121</subfield><subfield code="g">10</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
author |
Gu, Huijie |
spellingShingle |
Gu, Huijie ddc 570 ddc 610 bkl 44.44 Elsevier JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
authorStr |
Gu, Huijie |
ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV011050691 |
format |
electronic Article |
dewey-ones |
570 - Life sciences; biology 610 - Medicine & health |
delete_txt_mv |
keep |
author_role |
aut |
collection |
elsevier |
remote_str |
true |
illustrated |
Not Illustrated |
topic_title |
570 570 DE-600 610 VZ 44.44 bkl Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis Elsevier |
topic |
ddc 570 ddc 610 bkl 44.44 Elsevier JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis |
topic_unstemmed |
ddc 570 ddc 610 bkl 44.44 Elsevier JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis |
topic_browse |
ddc 570 ddc 610 bkl 44.44 Elsevier JNK Elsevier Human adipose-derived mesenchymal stem cells Elsevier Osteogenesis Elsevier Adipogenesis |
format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
format_main_str_mv |
Text Zeitschrift/Artikel |
carriertype_str_mv |
zu |
author2_variant |
z h zh x y xy j z jz l g lg j c jc k r kr j x jx l l ll l c lc |
hierarchy_parent_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
hierarchy_parent_id |
ELV011050691 |
dewey-tens |
570 - Life sciences; biology 610 - Medicine & health |
hierarchy_top_title |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
isfreeaccess_txt |
false |
familylinks_str_mv |
(DE-627)ELV011050691 |
title |
Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
ctrlnum |
(DE-627)ELV023966513 (ELSEVIER)S0014-4827(15)30067-7 |
title_full |
Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
author_sort |
Gu, Huijie |
journal |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
journalStr |
72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS |
lang_code |
eng |
isOA_bool |
false |
dewey-hundreds |
500 - Science 600 - Technology |
recordtype |
marc |
publishDateSort |
2015 |
contenttype_str_mv |
zzz |
container_start_page |
112 |
author_browse |
Gu, Huijie |
container_volume |
339 |
physical |
10 |
class |
570 570 DE-600 610 VZ 44.44 bkl |
format_se |
Elektronische Aufsätze |
author-letter |
Gu, Huijie |
doi_str_mv |
10.1016/j.yexcr.2015.08.005 |
dewey-full |
570 610 |
title_sort |
role of c-jun n-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
title_auth |
Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
abstract |
Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. |
abstractGer |
Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. |
abstract_unstemmed |
Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs. |
collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA GBV_ILN_70 |
container_issue |
1 |
title_short |
Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells |
url |
https://doi.org/10.1016/j.yexcr.2015.08.005 |
remote_bool |
true |
author2 |
Huang, Zhongyue Yin, Xiaofan Zhang, Jieping Gong, Lunli Chen, Jiong Rong, Ke Xu, Jun Lu, Lixia Cui, Lei |
author2Str |
Huang, Zhongyue Yin, Xiaofan Zhang, Jieping Gong, Lunli Chen, Jiong Rong, Ke Xu, Jun Lu, Lixia Cui, Lei |
ppnlink |
ELV011050691 |
mediatype_str_mv |
z |
isOA_txt |
false |
hochschulschrift_bool |
false |
author2_role |
oth oth oth oth oth oth oth oth oth |
doi_str |
10.1016/j.yexcr.2015.08.005 |
up_date |
2024-07-06T20:11:49.300Z |
_version_ |
1803861842250956800 |
fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV023966513</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625141948.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180603s2015 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.yexcr.2015.08.005</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBVA2015021000009.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV023966513</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0014-4827(15)30067-7</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.44</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Gu, Huijie</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Role of c-Jun N-terminal kinase in the osteogenic and adipogenic differentiation of human adipose-derived mesenchymal stem cells</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2015transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">10</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Although previous studies have characterized the osteogenic potential of adipose-derived mesenchymal stem cells (AMSCs) in vitro and in vivo, the molecular mechanism involved remains to be fully determined. Previously, we demonstrated that the ERK pathway plays an important role in osteogenesis and regulation of the balance between osteogenesis and adipogenesis. Here, we explored the possible role of JNKs in osteogenesis and adipogenesis of AMSCs. JNK activation in osteo-induced AMSCs was initiated at 15min, peaked at 30min, and declined from 45min to basal levels. Inhibition of the JNK signaling pathway using SP600125 blocked osteogenic differentiation in a dose-dependent manner, which was revealed by an ALP activity assay, extracellular calcium deposition detection, and expression of osteogenesis-relative genes (Runx2, ALP, and OCN) via RT-PCR and real-time PCR. However, blockage of JNK did not induce a switch between osteogenesis and adipogenesis of AMSCs in the presence of dexamethasone, which is different from that of blockage of ERK. Significantly, the blockage of JNK activation in adipo-induced AMSCs by SP600125 stimulated adipogenic differentiation, which was confirmed by Oil Red O staining to detect intracellular lipid droplets, and RT-PCR and real-time PCR analysis for expression of adipogenesis-relative genes (PPARγ2 and aP2). This study suggested a potential function of the JNK pathway in committing osteogenic and adipogenic differentiation of AMSCs in vitro. However, blockage of the JNK pathway is not sufficient to induce a switch from osteogenesis to adipogenesis of AMSCs.</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">JNK</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Human adipose-derived mesenchymal stem cells</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Osteogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="650" ind1=" " ind2="7"><subfield code="a">Adipogenesis</subfield><subfield code="2">Elsevier</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Huang, Zhongyue</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yin, Xiaofan</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zhang, Jieping</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Gong, Lunli</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Chen, Jiong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Rong, Ke</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Xu, Jun</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lu, Lixia</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Cui, Lei</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Academic Press</subfield><subfield code="t">72 OUTCOMES OF COMBINATION OF HEPATITIS B IMMUNOGLOBULIN AND HEPATITIS B VACCINATION IN HIGH-RISK NEWBORNS BORN TO HBEAG-POSITIVE MOTHERS</subfield><subfield code="d">2012</subfield><subfield code="d">ECR</subfield><subfield code="g">Orlando, Fla</subfield><subfield code="w">(DE-627)ELV011050691</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:339</subfield><subfield code="g">year:2015</subfield><subfield code="g">number:1</subfield><subfield code="g">day:15</subfield><subfield code="g">month:11</subfield><subfield code="g">pages:112-121</subfield><subfield code="g">extent:10</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.yexcr.2015.08.005</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ILN_70</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">44.44</subfield><subfield code="j">Parasitologie</subfield><subfield code="x">Medizin</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">339</subfield><subfield code="j">2015</subfield><subfield code="e">1</subfield><subfield code="b">15</subfield><subfield code="c">1115</subfield><subfield code="h">112-121</subfield><subfield code="g">10</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
|
score |
7.40007 |