Connective tissue growth factor induces cardiac hypertrophy through Akt signaling

被引：85

作者：

Hayata, Nozomi ^{[1
]}

Fujio, Yasushi ^{[1
]}

Yamamoto, Yasuhiro ^{[1
]}

Iwakura, Tomohiko ^{[1
]}

Obana, Masanori ^{[1
]}

Takai, Mika ^{[1
]}

Mohri, Tomomi ^{[1
]}

Nonen, Shinpei ^{[1
]}

Maeda, Makiko ^{[1
]}

Azuma, Junichi ^{[1
]}

机构：

[1] Osaka Univ, Grad Sch Pharmaceut Sci, Dept Clin Pharmacol & Pharmacogenom, Suita, Osaka 5650871, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2008年 / 370卷 / 02期

关键词：

connective tissue growth factor; CCN family; cardiac myocyte; hypertrophy; Akt;

D O I：

10.1016/j.bbrc.2008.03.100

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

In the process of cardiac remodeling, connective tissue growth factor (CTGF/CCN2) is secreted from cardiac myocytes. Though CTGF is well known to promote fibroblast proliferation, its pathophysiological effects in cardiac myocytes remain to be elucidated. In this study, we examined the biological effects of CTGF in rat neonatal cardiomyocytes. Cardiac myocytes stimulated with full length CTGF and its C-terminal region peptide showed the increase in cell surface area. Similar to hypertrophic ligands for G-protein coupled receptors, such as endothelin-1, CTGF activated amino acid uptake; however, CTGF-induced hypertrophy is not associated with the increased expression of skeletal actin or BNP, analyzed by Northern-blotting. CTGF treatment activated ERK1/2, p38 MAPK, JNK and Akt. The inhibition of Akt by transducing dominant-negative Akt abrogated CTGF-mediated increase in cell size, while the inhibition of MAP kinases did not affect the cardiac hypertrophy. These findings indicate that CTGF is a novel hypertrophic factor in cardiac myocytes. (C) 2008 Elsevier Inc. All rights reserved.

引用

页码：274 / 278

页数：5

共 22 条

[1] Connective-tissue growth factor - a novel mediator of angiotensin II-stimulated cardiac fibroblast activation in heart failure in rats [J].