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Recent studies have demonstrated that PR957 Akt plays important roles in the determination of cell size both in vitro and in vivo [17]. Therefore, we examined the effects of the inhibition of Akt by using adenovirus vector expressing dominant-negative Akt (dnAkt). Adenoviral transfer of dnAkt inhibited CTGF-mediated cardiomyocyte hypertrophy, while the transfection of adenovirus vetor expressing β-gal showed no effects ( Fig. 4B).
Discussion
In the present study, we demonstrated that full length of recombinant human CTGF induced cardiac hypertrophy in cultured cardiomyocytes. The C-terminal region of CTGF exhibited the similar effects in cardiac myocytes. However, neither skeletal actin nor BNP mRNA was upregulated by CTGF, unlike GPCR ligands such as ET-1. CTGF rapidly activated p38 MAPK, ERK1/2, JNK, and Akt. Inhibition of Akt by adenoviral transduction of dnAkt ameliorated CTGF-mediated cardiomyocyte hypertrophy. These data suggest that CTGF induces cardiomyocyte hypertrophy through Akt pathway.
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We found interesting results comparing mean expression levels in
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