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Text
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URL Address
<a href="http://doi.org/10.1042/cs20070160" target="_blank" rel="noreferrer noopener">http://doi.org/10.1042/cs20070160</a>
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Pages
357-364
Issue
7
Volume
113
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Title
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Ace2 Overexpression Inhibits Hypoxia-induced Collagen Production By Cardiac Fibroblasts
Publisher
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Clinical Science
Date
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2007
2007-10
Subject
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angiotensin-converting enzyme 2 (ACE2); angiotensin-converting enzyme-2; collagen; cross-talk; expression; fibroblast; growth-factor-beta; heart failure; hypoxia; Myocardial infarction; myofibroblast differentiation; oxidative stress; pathways; rat; remodelling; Research & Experimental Medicine; signaling; transforming growth factor beta (TGF beta)
Creator
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Grobe J L; Der Sarkissian S; Stewart J M; Meszaros J G; Raizada M K; Katovich M J
Description
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Cardiac remodelling is a key risk factor for the development of heart failure in the chronic phase following myocardial infarction. Our previous studies have shown an anti-remodelling role of ACE2 (angiotensin-converting enzyme 2) in vivo during hypertension and that these protective effects are mediated through increased circulating levels of Ang-(1-7) [angiotensin-(1-7)]. In the present study, we have demonstrated that cardiac myocytes have modest ACE2 activity, whereas cardiac fibroblasts do not: exhibit any endogenous activity. As fibroblasts are the major cell type found in an infarct zone following a myocardial infarction, we examined the effects of ACE2 gene delivery to cultured cardiac fibroblasts after acute hypoxic exposure. Cardiac fibroblasts from 5-day-old Sprague-Dawley rat hearts were grown to confluence and transduced with a lentiviral vector containing murine ACE2 cDNA under transcriptional control by the EFI alpha (elongation factor I alpha) promoter (lenti-ACE2). Transduction of fibroblasts with lenti-ACE2 resulted in a viral dose-dependent increase in ACE2 activity. This was associated with a significant attenuation of both basal and hypoxia/re-oxygenation-induced collagen production by the fibroblasts. Cytokine production, specifically TGF beta (transforming growth factor beta), by these cells was also significantly attenuated by ACE2 expression. Collectively, these results indicate that: (i) endogenous ACE2 activity is observed in cardiac myocytes, but not in cardiac fibroblasts; (ii) ACE2 overexpression in the cardiac fibroblast attenuates collagen production; and (iii) this prevention is probably mediated by decreased expression of cytokines. We conclude that ACE2 expression, limited to cardiac fibroblasts, may represent a novel paradigm for in vivo therapy following acute ischaemia.
Identifier
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<a href="http://doi.org/10.1042/cs20070160" target="_blank" rel="noreferrer noopener">10.1042/cs20070160</a>
Format
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Journal Article or Conference Abstract Publication
2007
angiotensin-converting enzyme 2 (ACE2)
angiotensin-converting enzyme-2
Clinical Science
Collagen
cross-talk
Der Sarkissian S
expression
fibroblast
Grobe J L
growth-factor-beta
Heart failure
hypoxia
Journal Article or Conference Abstract Publication
Katovich M J
Meszaros J G
myocardial infarction
myofibroblast differentiation
Oxidative Stress
pathways
Raizada M K
rat
remodelling
Research & Experimental Medicine
Signaling
Stewart J M
transforming growth factor beta (TGF beta)