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Connective tissue growth factor induces cardiac hypertrophy through Akt signaling.

Abstract：

: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.

journal_name

Biochem Biophys Res Commun

journal_title

Biochemical and biophysical research communications

authors

Hayata N,Fujio Y,Yamamoto Y,Iwakura T,Obana M,Takai M,Mohri T,Nonen S,Maeda M,Azuma J

doi

10.1016/j.bbrc.2008.03.100

subject

Has Abstract

pub_date

2008-05-30 00:00:00

pages

274-8

issue

2

eissn

0006-291X

issn

1090-2104

pii

S0006-291X(08)00550-0

journal_volume

370

pub_type

杂志文章

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