Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and...
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Autor*in:	Gao, Lilan [verfasserIn] Li, Shengchun [verfasserIn] Wei, Xiaochun [verfasserIn] Du, Guoqing [verfasserIn] Wei, Dennis [verfasserIn] Wei, Lei [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2020

Schlagwörter:	Histone deacetylase 4 Growth plate Mice Chondrocytes Angiogenesis

Übergeordnetes Werk:	Enthalten in: Molecular medicine - [London] : BioMed Central, 1994, 26(2020), 1 vom: 01. Mai
Übergeordnetes Werk:	volume:26 ; year:2020 ; number:1 ; day:01 ; month:05

Links:	Volltext

DOI / URN:	10.1186/s10020-020-00154-6

Katalog-ID:	SPR039583643

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520			\|a Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.
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allfields	10.1186/s10020-020-00154-6 doi (DE-627)SPR039583643 (SPR)s10020-020-00154-6-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl Gao, Lilan verfasserin aut Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates. Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Li, Shengchun verfasserin aut Wei, Xiaochun verfasserin aut Du, Guoqing verfasserin aut Wei, Dennis verfasserin aut Wei, Lei verfasserin aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 26(2020), 1 vom: 01. Mai (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:26 year:2020 number:1 day:01 month:05 https://dx.doi.org/10.1186/s10020-020-00154-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 26 2020 1 01 05
spelling	10.1186/s10020-020-00154-6 doi (DE-627)SPR039583643 (SPR)s10020-020-00154-6-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl Gao, Lilan verfasserin aut Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates. Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Li, Shengchun verfasserin aut Wei, Xiaochun verfasserin aut Du, Guoqing verfasserin aut Wei, Dennis verfasserin aut Wei, Lei verfasserin aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 26(2020), 1 vom: 01. Mai (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:26 year:2020 number:1 day:01 month:05 https://dx.doi.org/10.1186/s10020-020-00154-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 26 2020 1 01 05
allfields_unstemmed	10.1186/s10020-020-00154-6 doi (DE-627)SPR039583643 (SPR)s10020-020-00154-6-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl Gao, Lilan verfasserin aut Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates. Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Li, Shengchun verfasserin aut Wei, Xiaochun verfasserin aut Du, Guoqing verfasserin aut Wei, Dennis verfasserin aut Wei, Lei verfasserin aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 26(2020), 1 vom: 01. Mai (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:26 year:2020 number:1 day:01 month:05 https://dx.doi.org/10.1186/s10020-020-00154-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 26 2020 1 01 05
allfieldsGer	10.1186/s10020-020-00154-6 doi (DE-627)SPR039583643 (SPR)s10020-020-00154-6-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl Gao, Lilan verfasserin aut Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates. Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Li, Shengchun verfasserin aut Wei, Xiaochun verfasserin aut Du, Guoqing verfasserin aut Wei, Dennis verfasserin aut Wei, Lei verfasserin aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 26(2020), 1 vom: 01. Mai (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:26 year:2020 number:1 day:01 month:05 https://dx.doi.org/10.1186/s10020-020-00154-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 26 2020 1 01 05
allfieldsSound	10.1186/s10020-020-00154-6 doi (DE-627)SPR039583643 (SPR)s10020-020-00154-6-e DE-627 ger DE-627 rakwb eng 610 ASE 610 ASE 44.00 bkl Gao, Lilan verfasserin aut Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo 2020 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates. Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213 Li, Shengchun verfasserin aut Wei, Xiaochun verfasserin aut Du, Guoqing verfasserin aut Wei, Dennis verfasserin aut Wei, Lei verfasserin aut Enthalten in Molecular medicine [London] : BioMed Central, 1994 26(2020), 1 vom: 01. Mai (DE-627)269539611 (DE-600)1475577-4 1528-3658 nnns volume:26 year:2020 number:1 day:01 month:05 https://dx.doi.org/10.1186/s10020-020-00154-6 kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_206 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2153 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 44.00 ASE AR 26 2020 1 01 05
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To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. 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author	Gao, Lilan
spellingShingle	Gao, Lilan ddc 610 bkl 44.00 misc Histone deacetylase 4 misc Growth plate misc Mice misc Chondrocytes misc Angiogenesis Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
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topic_title	610 ASE 44.00 bkl Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo Histone deacetylase 4 (dpeaa)DE-He213 Growth plate (dpeaa)DE-He213 Mice (dpeaa)DE-He213 Chondrocytes (dpeaa)DE-He213 Angiogenesis (dpeaa)DE-He213
topic	ddc 610 bkl 44.00 misc Histone deacetylase 4 misc Growth plate misc Mice misc Chondrocytes misc Angiogenesis
topic_unstemmed	ddc 610 bkl 44.00 misc Histone deacetylase 4 misc Growth plate misc Mice misc Chondrocytes misc Angiogenesis
topic_browse	ddc 610 bkl 44.00 misc Histone deacetylase 4 misc Growth plate misc Mice misc Chondrocytes misc Angiogenesis
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title	Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
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title_full	Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
author_sort	Gao, Lilan
journal	Molecular medicine
journalStr	Molecular medicine
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author_browse	Gao, Lilan Li, Shengchun Wei, Xiaochun Du, Guoqing Wei, Dennis Wei, Lei
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title_sort	conditional deletion of hdac4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
title_auth	Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
abstract	Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.
abstractGer	Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.
abstract_unstemmed	Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. Conclusions HDAC4 expression in chondrocytes contributes to angiogenesis in the growth plate, and its absence in vivo negatively affects growth plates.
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title_short	Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo
url	https://dx.doi.org/10.1186/s10020-020-00154-6
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author2	Li, Shengchun Wei, Xiaochun Du, Guoqing Wei, Dennis Wei, Lei
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up_date	2024-07-04T00:36:43.515Z
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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">SPR039583643</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519155821.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2020 xx \|\|\|\|\|o 00\| \|\|eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1186/s10020-020-00154-6</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR039583643</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s10020-020-00154-6-e</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="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">ASE</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">44.00</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Gao, Lilan</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">Text</subfield><subfield code="b">txt</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">Computermedien</subfield><subfield code="b">c</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">Online-Ressource</subfield><subfield code="b">cr</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background HDAC4 is a key regulator of chondrocyte hypertrophy and skeletal development, but it is not clear whether the increase in vascular invasion at growth plates is related to HDAC4 expression. To determine it, we investigated the relationship between HDAC4 and angiogenesis in both in vivo and in vitro models. Methods HDAC4 was deleted in Col2α1-Cre; $ HDAC4^{fl/fl} $ mice. Growth of the Col2α1-Cre; $ HDAC4^{d/d} $ mice was compared with $ HDAC4^{fl/fl} $ mice at postnatal days 2, 4, 6, and 8. X-rays were taken to examine skeletal development. At postnatal days 14 and 21, mice were euthanized for specimen collection. Murine chondrocytes were isolated from the ventral parts of rib cages of 6-day-old mice (C57Bl/6) and transfected with a vector expressing HDAC4 as a fusion protein with green fluorescent protein (GFP). Relative expression levels of HDAC4, VEGF, and Hif1α were measured in these cells by Western blot, RT-qPCR, enzyme-linked immunosorbent, histology, and immunohistochemistry assays. Results The Col2α1-Cre; $ HDAC4^{d/d} $ mice were markedly smaller compared with the control mice. At postnatal days 14 and 21, the Col2α1-Cre; $ HDAC4^{d/d} $ mice exhibited a shortened growth plate, a larger secondary ossification center, and stronger staining of CD31 and CD34 compared to control mice. The isolated chondrocyte cells exhibited a high transfection efficiency of HDAC4 which resulted in the detection of a significant decrease in VEGF and Hif1α levels compared with the control chondrocytes. 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Conditional deletion of HDAC4 from collagen type 2α1-expressing cells increases angiogenesis in vivo

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