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Upregulation Of Angiotensin Converting Enzyme 2 In Hepatic Fibrosis By Angiotensin Converting Enzyme Inhibitors: An In Vivo And In Vitro Study.

Authors: Huang, ML  Li, X  Meng, Y  Xiao, B  Ma, Q  Ying, SS  Wu, PS  Zhang, ZS 
Citation: Huang ML, etal., Clin Exp Pharmacol Physiol. 2009 Sep 28.
Pubmed: (View Article at PubMed) PMID:19793108
DOI: Full-text: DOI:10.1111/j.1440-1681.2009.05302.x

Summary 1. The role of angiotensin converting enzyme 2 (ACE2) is likely to balance the status of the renin angiotensin system (RAS) by degrading angiotensin (Ang) II and generating Ang-(1-7). Earlier demonstrations that ACE2 is insensitive to ACE inhibitors (ACEI) prompted us to evaluate the effect of ACEI on ACE2 expression. 2. The mRNA levels of ACE2 and the Ang-(1-7) receptor Mas, as well as levels of ACE2 protein, were measured in carbon tetrachloride (CCl(4))-injured rat liver and in Ang II- treated hepatic stellate cells (HSCs). The effects of ACEI on ACE2 expression and Mas mRNA levels were concomitantly assessed and further evaluated with respect to Mas receptor antagonism. 3. ACE2 expression and Mas mRNA levels were markedly upregulated in CCl(4)-injured rat liver and in Ang II-treated HSCs. Further significant upregulation was observed following additional administration of ACEI. ACEI treatment of HSCs inhibited Ang II-induced connective tissue growth factor (CTGF) overexpression and this effect could be reduced by a blockage of the Mas receptor. 4. These findings suggest that ACEI is able to upregulate ACE2 under conditions of liver injury both in vivo and in vitro, which may indicate potential benefits of ACEI in the therapeutic treatment of liver fibrosis.


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CRRD Object Information
CRRD ID: 2316776
Created: 2010-02-23
Species: All species
Last Modified: 2010-02-23
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.