CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice

Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Metho...
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Gespeichert in:

Autor*in:	Cheng-Wei Xu [verfasserIn] Tian-Peng Zhang [verfasserIn] Hong-Xia Wang [verfasserIn] Hui Yang [verfasserIn] Hui-Hua Li [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2013

Schlagwörter:	Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction

Übergeordnetes Werk:	In: Cellular Physiology and Biochemistry - Cell Physiol Biochem Press GmbH & Co KG, 2002, 31(2013), 2-3, Seite 199-208
Übergeordnetes Werk:	volume:31 ; year:2013 ; number:2-3 ; pages:199-208

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc Journal toc

DOI / URN:	10.1159/000343361

Katalog-ID:	DOAJ075887541

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520			\|a Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI.
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650		4	\|a Myocardial infarction
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allfields	10.1159/000343361 doi (DE-627)DOAJ075887541 (DE-599)DOAJ0c648dd90a9946ecb7890ac32b4e59a7 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Cheng-Wei Xu verfasserin aut CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI. Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction Physiology Biochemistry Tian-Peng Zhang verfasserin aut Hong-Xia Wang verfasserin aut Hui Yang verfasserin aut Hui-Hua Li verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 31(2013), 2-3, Seite 199-208 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:31 year:2013 number:2-3 pages:199-208 https://doi.org/10.1159/000343361 kostenfrei https://doaj.org/article/0c648dd90a9946ecb7890ac32b4e59a7 kostenfrei http://www.karger.com/Article/FullText/343361 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 AR 31 2013 2-3 199-208
spelling	10.1159/000343361 doi (DE-627)DOAJ075887541 (DE-599)DOAJ0c648dd90a9946ecb7890ac32b4e59a7 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Cheng-Wei Xu verfasserin aut CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI. Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction Physiology Biochemistry Tian-Peng Zhang verfasserin aut Hong-Xia Wang verfasserin aut Hui Yang verfasserin aut Hui-Hua Li verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 31(2013), 2-3, Seite 199-208 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:31 year:2013 number:2-3 pages:199-208 https://doi.org/10.1159/000343361 kostenfrei https://doaj.org/article/0c648dd90a9946ecb7890ac32b4e59a7 kostenfrei http://www.karger.com/Article/FullText/343361 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 AR 31 2013 2-3 199-208
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allfieldsGer	10.1159/000343361 doi (DE-627)DOAJ075887541 (DE-599)DOAJ0c648dd90a9946ecb7890ac32b4e59a7 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Cheng-Wei Xu verfasserin aut CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI. Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction Physiology Biochemistry Tian-Peng Zhang verfasserin aut Hong-Xia Wang verfasserin aut Hui Yang verfasserin aut Hui-Hua Li verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 31(2013), 2-3, Seite 199-208 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:31 year:2013 number:2-3 pages:199-208 https://doi.org/10.1159/000343361 kostenfrei https://doaj.org/article/0c648dd90a9946ecb7890ac32b4e59a7 kostenfrei http://www.karger.com/Article/FullText/343361 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 AR 31 2013 2-3 199-208
allfieldsSound	10.1159/000343361 doi (DE-627)DOAJ075887541 (DE-599)DOAJ0c648dd90a9946ecb7890ac32b4e59a7 DE-627 ger DE-627 rakwb eng QP1-981 QD415-436 Cheng-Wei Xu verfasserin aut CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice 2013 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI. Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction Physiology Biochemistry Tian-Peng Zhang verfasserin aut Hong-Xia Wang verfasserin aut Hui Yang verfasserin aut Hui-Hua Li verfasserin aut In Cellular Physiology and Biochemistry Cell Physiol Biochem Press GmbH & Co KG, 2002 31(2013), 2-3, Seite 199-208 (DE-627)300189702 (DE-600)1482056-0 14219778 nnns volume:31 year:2013 number:2-3 pages:199-208 https://doi.org/10.1159/000343361 kostenfrei https://doaj.org/article/0c648dd90a9946ecb7890ac32b4e59a7 kostenfrei http://www.karger.com/Article/FullText/343361 kostenfrei https://doaj.org/toc/1015-8987 Journal toc kostenfrei https://doaj.org/toc/1421-9778 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ 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_69 GBV_ILN_70 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_374 GBV_ILN_602 GBV_ILN_2014 GBV_ILN_2018 GBV_ILN_2153 GBV_ILN_2885 GBV_ILN_2886 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 AR 31 2013 2-3 199-208
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Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. 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callnumber-first	Q - Science
author	Cheng-Wei Xu
spellingShingle	Cheng-Wei Xu misc QP1-981 misc QD415-436 misc Carboxyl terminus of Hsp70-interacting protein misc Myocardial infarction misc Angiogenesis misc Apoptosis misc Inflammation misc Cardiac dysfunction misc Physiology misc Biochemistry CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice
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topic_title	QP1-981 QD415-436 CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice Carboxyl terminus of Hsp70-interacting protein Myocardial infarction Angiogenesis Apoptosis Inflammation Cardiac dysfunction
topic	misc QP1-981 misc QD415-436 misc Carboxyl terminus of Hsp70-interacting protein misc Myocardial infarction misc Angiogenesis misc Apoptosis misc Inflammation misc Cardiac dysfunction misc Physiology misc Biochemistry
topic_unstemmed	misc QP1-981 misc QD415-436 misc Carboxyl terminus of Hsp70-interacting protein misc Myocardial infarction misc Angiogenesis misc Apoptosis misc Inflammation misc Cardiac dysfunction misc Physiology misc Biochemistry
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title	CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice
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title_full	CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice
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title_sort	chip enhances angiogenesis and restores cardiac function after infarction in transgenic mice
callnumber	QP1-981
title_auth	CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice
abstract	Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI.
abstractGer	Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI.
abstract_unstemmed	Background: Carboxyl terminus of Hsp70-interacting protein (CHIP) is a chaperone/ubiquitin ligase that plays an important role in stress-induced apoptosis. However, the effect of CHIP on angiogenesis, cardiac function and survival 4 weeks after myocardial infarction (MI) remain to be explored. Methods: Wild-type (WT) and transgenic mice (TG) with cardiac-specific overexpression of CHIP were used for coronary artery ligation. The cardiac function, cardiomyocyte apoptosis, inflammation and angiogenesis were examined by echocardiography, histological analysis, real-time PCR and Western blot analysis. Results: At 4 weeks of after coronary artery ligation, echocardiography demonstrated that cardiac remodeling and dysfunction were prevented in TG mice compared with WT mice. The infarct size, cardiomyocyte apoptosis and inflammation were significantly reduced in TG mice than in WT mice. The survival rate after MI in TG mice was higher than that of WT mice. Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. Thus, increased CHIP level may provide a novel therapeutic approach for left ventricular dysfunction after MI.
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title_short	CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice
url	https://doi.org/10.1159/000343361 https://doaj.org/article/0c648dd90a9946ecb7890ac32b4e59a7 http://www.karger.com/Article/FullText/343361 https://doaj.org/toc/1015-8987 https://doaj.org/toc/1421-9778
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up_date	2024-07-03T17:23:47.204Z
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Furthermore, the levels of p53 protein was markedly decreased, but the expression of HIF-1α and VEGF, and the formation of capillary and arteriole after MI were significantly enhanced in TG mice compared with WT mice. Conclusion: We report the first in vivo evidence that CHIP enhances angiogenesis, inhibits inflammation, restores cardiac function, and improves survival at 4 weeks after MI. The present study expands on previous results and defines a novel mechanism. 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CHIP Enhances Angiogenesis and Restores Cardiac Function After Infarction in Transgenic Mice

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