The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.

<h4>Background</h4>Integrin linked kinase (ILK), as an important component of mechanical stretch sensor, can initiate cellular signaling response in the heart when cardiac preload increases. Previous work demonstrated increased ILK expression could induce angiogenesis to improved heart f...

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Autores principales:	Jun Xie, Wen Lu, Rong Gu, Qin Dai, Bin Zong, Lin Ling, Biao Xu
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2011
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/489e6fe81dbb49ffa77b174004258e65
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spelling	oai:doaj.org-article:489e6fe81dbb49ffa77b174004258e652021-11-04T06:08:25ZThe impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.1932-620310.1371/journal.pone.0024115https://doaj.org/article/489e6fe81dbb49ffa77b174004258e652011-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/21949693/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Background</h4>Integrin linked kinase (ILK), as an important component of mechanical stretch sensor, can initiate cellular signaling response in the heart when cardiac preload increases. Previous work demonstrated increased ILK expression could induce angiogenesis to improved heart function after MI. However the patholo-physiological role of ILK in cardiac remodeling after MI is not clear.<h4>Method and results</h4>Hearts were induced to cardiac remodeling by infarction and studied in Sprague-Dawley rats. Until 4 weeks after infarction, ILK expression was increased in non-ischemic tissue in parallel with myocytes hypertrophy and compensatory cardiac function. 8 weeks later, when decompensation of heart function occurred, ILK level returned to baseline. Followed ILK alternation, vascular endothelial growth factor (VEGF) expression and phosphorylation of endothelial nitric oxide synthase (eNOS) was significantly decreased 8 weeks after MI. Histology study also showed significantly microvessel decreased and myocytes loss 8 weeks paralleled with ILK down-regulation. While ILK expression was maintained by gene delivery, tissue angiogenesis and cardiac function was preserved during cardiac remodeling.<h4>Conclusion</h4>Temporally up-regulation of ILK level in non-ischemic myocytes by increased external load is associated with beneficial angiogenesis to maintain infarction-induced cardiac hypertrophy. When ILK expression returns to normal, this cardiac adaptive response for infarction is weaken. Understanding the ILK related mechanism of cardiac maladaptation leads to a new strategy for treatment of heart failure after infarction.Jun XieWen LuRong GuQin DaiBin ZongLin LingBiao XuPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 6, Iss 9, p e24115 (2011)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Jun Xie Wen Lu Rong Gu Qin Dai Bin Zong Lin Ling Biao Xu The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
description	<h4>Background</h4>Integrin linked kinase (ILK), as an important component of mechanical stretch sensor, can initiate cellular signaling response in the heart when cardiac preload increases. Previous work demonstrated increased ILK expression could induce angiogenesis to improved heart function after MI. However the patholo-physiological role of ILK in cardiac remodeling after MI is not clear.<h4>Method and results</h4>Hearts were induced to cardiac remodeling by infarction and studied in Sprague-Dawley rats. Until 4 weeks after infarction, ILK expression was increased in non-ischemic tissue in parallel with myocytes hypertrophy and compensatory cardiac function. 8 weeks later, when decompensation of heart function occurred, ILK level returned to baseline. Followed ILK alternation, vascular endothelial growth factor (VEGF) expression and phosphorylation of endothelial nitric oxide synthase (eNOS) was significantly decreased 8 weeks after MI. Histology study also showed significantly microvessel decreased and myocytes loss 8 weeks paralleled with ILK down-regulation. While ILK expression was maintained by gene delivery, tissue angiogenesis and cardiac function was preserved during cardiac remodeling.<h4>Conclusion</h4>Temporally up-regulation of ILK level in non-ischemic myocytes by increased external load is associated with beneficial angiogenesis to maintain infarction-induced cardiac hypertrophy. When ILK expression returns to normal, this cardiac adaptive response for infarction is weaken. Understanding the ILK related mechanism of cardiac maladaptation leads to a new strategy for treatment of heart failure after infarction.
format	article
author	Jun Xie Wen Lu Rong Gu Qin Dai Bin Zong Lin Ling Biao Xu
author_facet	Jun Xie Wen Lu Rong Gu Qin Dai Bin Zong Lin Ling Biao Xu
author_sort	Jun Xie
title	The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
title_short	The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
title_full	The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
title_fullStr	The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
title_full_unstemmed	The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.
title_sort	impairment of ilk related angiogenesis involved in cardiac maladaptation after infarction.
publisher	Public Library of Science (PLoS)
publishDate	2011
url	https://doaj.org/article/489e6fe81dbb49ffa77b174004258e65
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The impairment of ILK related angiogenesis involved in cardiac maladaptation after infarction.

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