Cellular repressor of E1A-stimulated genes attenuates cardiac hypertrophy and fibrosis

DSpace/Manakin Repository

Cellular repressor of E1A-stimulated genes attenuates cardiac hypertrophy and fibrosis

Citable link to this page

 

 
Title: Cellular repressor of E1A-stimulated genes attenuates cardiac hypertrophy and fibrosis
Author: Bian, Zhouyan; Cai, Jun; Shen, Di-fei; Chen, Li; Yan, Ling; Tang, Qizhu; Li, Hongliang

Note: Order does not necessarily reflect citation order of authors.

Citation: Bian, Zhouyan, Jun Cai, Di-fei Shen, Li Chen, Ling Yan, Qizhu Tang, and Hongliang Li. 2009. “Cellular repressor of E1A-stimulated genes attenuates cardiac hypertrophy and fibrosis.” Journal of Cellular and Molecular Medicine 13 (7): 1302-1313. doi:10.1111/j.1582-4934.2008.00633.x. http://dx.doi.org/10.1111/j.1582-4934.2008.00633.x.
Full Text & Related Files:
Abstract: Cellular repressor of E1A-stimulated genes (CREG) is a secreted glycoprotein of 220 amino acids. It has been proposed that CREG acts as a ligand that enhances differentiation and/or reduces cell proliferation. CREG has been shown previously to attenuate cardiac hypertrophy in vitro. However, such a role has not been determined in vivo. In the present study, we tested the hypothesis that overexpression of CREG in the murine heart would protect against cardiac hypertrophy and fibrosis in vivo. The effects of constitutive human CREG expression on cardiac hypertrophy were investigated using both in vitro and in vivo models. Cardiac hypertrophy was produced by aortic banding and infusion of angiotensin II in CREG transgenic mice and control animals. The extent of cardiac hypertrophy was quantitated by two-dimensional and M-mode echocardiography as well as by molecular and pathological analyses of heart samples. Constitutive over-expression of human CREG in the murine heart attenuated the hypertrophic response, markedly reduced inflammation. Cardiac function was also preserved in hearts with increased CREG levels in response to hypertrophic stimuli. These beneficial effects were associated with attenuation of the mitogen-activated protein kinase (MAPK)-extracellular signal-regulated kinase 1 (MEK-ERK1)/2-dependent signalling cascade. In addition, CREG expression blocked fibrosis and collagen synthesis through blocking MEK-ERK1/2-dependent Smad 2/3 activation in vitro and in vivo. Therefore, the expression of CREG improves cardiac functions and inhibits cardiac hypertrophy, inflammation and fibrosis through blocking MEK-ERK1/2-dependent signalling.
Published Version: doi:10.1111/j.1582-4934.2008.00633.x
Other Sources: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4496144/pdf/
Terms of Use: This article is made available under the terms and conditions applicable to Other Posted Material, as set forth at http://nrs.harvard.edu/urn-3:HUL.InstRepos:dash.current.terms-of-use#LAA
Citable link to this page: http://nrs.harvard.edu/urn-3:HUL.InstRepos:17820950
Downloads of this work:

Show full Dublin Core record

This item appears in the following Collection(s)

 
 

Search DASH


Advanced Search
 
 

Submitters