HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway
Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Yan, Xuetao [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2018 |
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| Schlagwörter: |
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| Anmerkung: |
© Biomedical Engineering Society 2018 |
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| Übergeordnetes Werk: |
Enthalten in: Cellular and molecular bioengineering - New Yok, NY [u.a.] : Springer, 2008, 11(2018), 6 vom: 06. Sept., Seite 509-518 |
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| Übergeordnetes Werk: |
volume:11 ; year:2018 ; number:6 ; day:06 ; month:09 ; pages:509-518 |
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| DOI / URN: |
10.1007/s12195-018-0540-0 |
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| Katalog-ID: |
SPR025187384 |
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| 520 | |a Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. | ||
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| 650 | 4 | |a HO-1 overexpression |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a MSCs |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a JAK/stat3 pathway |7 (dpeaa)DE-He213 | |
| 650 | 4 | |a CFU |7 (dpeaa)DE-He213 | |
| 700 | 1 | |a Cheng, Xiaoli |4 aut | |
| 700 | 1 | |a He, Xianghu |4 aut | |
| 700 | 1 | |a Zheng, Wenzhong |4 aut | |
| 700 | 1 | |a Yuan, Xiaofang |4 aut | |
| 700 | 1 | |a Chen, Hu |4 aut | |
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10.1007/s12195-018-0540-0 doi (DE-627)SPR025187384 (SPR)s12195-018-0540-0-e DE-627 ger DE-627 rakwb eng Yan, Xuetao verfasserin (orcid)0000-0002-8745-4050 aut HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2018 Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 Cheng, Xiaoli aut He, Xianghu aut Zheng, Wenzhong aut Yuan, Xiaofang aut Chen, Hu aut Enthalten in Cellular and molecular bioengineering New Yok, NY [u.a.] : Springer, 2008 11(2018), 6 vom: 06. Sept., Seite 509-518 (DE-627)560179030 (DE-600)2416037-4 1865-5033 nnns volume:11 year:2018 number:6 day:06 month:09 pages:509-518 https://dx.doi.org/10.1007/s12195-018-0540-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 11 2018 6 06 09 509-518 |
| spelling |
10.1007/s12195-018-0540-0 doi (DE-627)SPR025187384 (SPR)s12195-018-0540-0-e DE-627 ger DE-627 rakwb eng Yan, Xuetao verfasserin (orcid)0000-0002-8745-4050 aut HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2018 Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 Cheng, Xiaoli aut He, Xianghu aut Zheng, Wenzhong aut Yuan, Xiaofang aut Chen, Hu aut Enthalten in Cellular and molecular bioengineering New Yok, NY [u.a.] : Springer, 2008 11(2018), 6 vom: 06. Sept., Seite 509-518 (DE-627)560179030 (DE-600)2416037-4 1865-5033 nnns volume:11 year:2018 number:6 day:06 month:09 pages:509-518 https://dx.doi.org/10.1007/s12195-018-0540-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 11 2018 6 06 09 509-518 |
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10.1007/s12195-018-0540-0 doi (DE-627)SPR025187384 (SPR)s12195-018-0540-0-e DE-627 ger DE-627 rakwb eng Yan, Xuetao verfasserin (orcid)0000-0002-8745-4050 aut HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2018 Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 Cheng, Xiaoli aut He, Xianghu aut Zheng, Wenzhong aut Yuan, Xiaofang aut Chen, Hu aut Enthalten in Cellular and molecular bioengineering New Yok, NY [u.a.] : Springer, 2008 11(2018), 6 vom: 06. Sept., Seite 509-518 (DE-627)560179030 (DE-600)2416037-4 1865-5033 nnns volume:11 year:2018 number:6 day:06 month:09 pages:509-518 https://dx.doi.org/10.1007/s12195-018-0540-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 11 2018 6 06 09 509-518 |
| allfieldsGer |
10.1007/s12195-018-0540-0 doi (DE-627)SPR025187384 (SPR)s12195-018-0540-0-e DE-627 ger DE-627 rakwb eng Yan, Xuetao verfasserin (orcid)0000-0002-8745-4050 aut HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2018 Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 Cheng, Xiaoli aut He, Xianghu aut Zheng, Wenzhong aut Yuan, Xiaofang aut Chen, Hu aut Enthalten in Cellular and molecular bioengineering New Yok, NY [u.a.] : Springer, 2008 11(2018), 6 vom: 06. Sept., Seite 509-518 (DE-627)560179030 (DE-600)2416037-4 1865-5033 nnns volume:11 year:2018 number:6 day:06 month:09 pages:509-518 https://dx.doi.org/10.1007/s12195-018-0540-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 11 2018 6 06 09 509-518 |
| allfieldsSound |
10.1007/s12195-018-0540-0 doi (DE-627)SPR025187384 (SPR)s12195-018-0540-0-e DE-627 ger DE-627 rakwb eng Yan, Xuetao verfasserin (orcid)0000-0002-8745-4050 aut HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway 2018 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © Biomedical Engineering Society 2018 Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 Cheng, Xiaoli aut He, Xianghu aut Zheng, Wenzhong aut Yuan, Xiaofang aut Chen, Hu aut Enthalten in Cellular and molecular bioengineering New Yok, NY [u.a.] : Springer, 2008 11(2018), 6 vom: 06. Sept., Seite 509-518 (DE-627)560179030 (DE-600)2416037-4 1865-5033 nnns volume:11 year:2018 number:6 day:06 month:09 pages:509-518 https://dx.doi.org/10.1007/s12195-018-0540-0 lizenzpflichtig Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2070 GBV_ILN_2086 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2116 GBV_ILN_2118 GBV_ILN_2119 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4012 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 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_4326 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4393 GBV_ILN_4700 AR 11 2018 6 06 09 509-518 |
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English |
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Enthalten in Cellular and molecular bioengineering 11(2018), 6 vom: 06. Sept., Seite 509-518 volume:11 year:2018 number:6 day:06 month:09 pages:509-518 |
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Enthalten in Cellular and molecular bioengineering 11(2018), 6 vom: 06. Sept., Seite 509-518 volume:11 year:2018 number:6 day:06 month:09 pages:509-518 |
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AKI HO-1 overexpression MSCs JAK/stat3 pathway CFU |
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Cellular and molecular bioengineering |
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Yan, Xuetao @@aut@@ Cheng, Xiaoli @@aut@@ He, Xianghu @@aut@@ Zheng, Wenzhong @@aut@@ Yuan, Xiaofang @@aut@@ Chen, Hu @@aut@@ |
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2018-09-06T00:00:00Z |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">SPR025187384</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230519222728.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">201007s2018 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1007/s12195-018-0540-0</subfield><subfield code="2">doi</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)SPR025187384</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(SPR)s12195-018-0540-0-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="100" ind1="1" ind2=" "><subfield code="a">Yan, Xuetao</subfield><subfield code="e">verfasserin</subfield><subfield code="0">(orcid)0000-0002-8745-4050</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2018</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="500" ind1=" " ind2=" "><subfield code="a">© Biomedical Engineering Society 2018</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. 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|
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Yan, Xuetao |
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Yan, Xuetao misc AKI misc HO-1 overexpression misc MSCs misc JAK/stat3 pathway misc CFU HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway |
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HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway AKI (dpeaa)DE-He213 HO-1 overexpression (dpeaa)DE-He213 MSCs (dpeaa)DE-He213 JAK/stat3 pathway (dpeaa)DE-He213 CFU (dpeaa)DE-He213 |
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HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway |
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HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway |
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Yan, Xuetao Cheng, Xiaoli He, Xianghu Zheng, Wenzhong Yuan, Xiaofang Chen, Hu |
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ho-1 overexpressed mesenchymal stem cells ameliorate sepsis-associated acute kidney injury by activating jak/stat3 pathway |
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HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway |
| abstract |
Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. © Biomedical Engineering Society 2018 |
| abstractGer |
Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. © Biomedical Engineering Society 2018 |
| abstract_unstemmed |
Background Stem cell therapy has been increasingly used in the treatment of sepsis-associated acute kidney injury (AKI). Engineering stem cells, through genetic method, for optimized therapeutic outcome is a desirable strategy, which requires clear understanding of molecular mechanism underlying the interaction between stem cells and damaged kidney. The aim of this study is to evaluate the therapeutic effects of HO-1 overexpressed mesenchymal stem cells (MSCs) in AKI and investigate the role of JAK/stat3 pathway in the treatment strategy. Method HO-1 was overexpressed in human MSCs with transfection of the expression plasmid. Quantitative RT-PCR was used to validate HO-1 overexpression. Sepsis was induced by the Cecal ligation and puncture (CLP) in mice. Survival of the treated mice were monitored and compared to that of the untreated mice. Biochemical analysis of serum biomarkers including colony forming unit (CFU), Creatinine (Cr) and blood urea nitrogen (BUN) was acquired and acute tubular necrosis (ATN) was measured. The extent of kidney injury was assessed through H&E staining of the kidney sections. Inflammatory factors were also compared between the two groups. Western blot was used to analyze the role of JAK/stat3 signaling pathway in this treatment strategy. Results MSCs with HO-1 overexpression markedly improved the survival of the AKI mice, accompanied by decreasing of CFU, Cr BUN in serum and ATN scores. H&E staining validated that kidney tissue demonstrated morphology that was similar to normal kidney in HO-1 MSC treated group. Inflammatory factors were also reduced by HO-1 MSC treatment. Western blot analysis indicated an upregulation of key proteins in the JAK/stat3 pathway. Conclusions HO-1 overexpression enhances therapeutic effect of MSCs in AKI, which is presumably attributed to the activation of JAK/stat3 signaling pathway. © Biomedical Engineering Society 2018 |
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| title_short |
HO-1 Overexpressed Mesenchymal Stem Cells Ameliorate Sepsis-Associated Acute Kidney Injury by Activating JAK/stat3 Pathway |
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https://dx.doi.org/10.1007/s12195-018-0540-0 |
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Cheng, Xiaoli He, Xianghu Zheng, Wenzhong Yuan, Xiaofang Chen, Hu |
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Cheng, Xiaoli He, Xianghu Zheng, Wenzhong Yuan, Xiaofang Chen, Hu |
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10.1007/s12195-018-0540-0 |
| up_date |
2024-07-03T14:25:34.467Z |
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| score |
7.4030848 |