Life Sciences 2002-01-01

Involvement of peptidyl-prolyl isomerase Pin1 in the inhibitory effect of fluvastatin on endothelin-1-induced cardiomyocyte hypertrophy

Satoshi Sakai, Nobutake Shimojo, Taizo Kimura, Kazuko Tajiri, Hidekazu Maruyama, Satoshi Homma, Keisuke Kuga, Taro Mizutani, Kazutaka Aonuma, Takashi Miyauchi

Index: Life Sci. 102(2) , 98-104, (2014)

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Abstract

Aims Cardiac hypertrophy is elicited by endothelin (ET)-1 as well as other neurohumoral factors, hemodynamic overload, and oxidative stress; HMG-CoA reductase inhibitors (statins) were shown to inhibit cardiac hypertrophy partly via the anti-oxidative stress. One of their common intracellular pathways is the phosphorylation cascade of MEK signaling. Pin1 specifically isomerizes the phosphorylated protein with Ser/Thr-Pro bonds and regulates their activity through conformational changes. There is no report whether the Pin1 activation contributes to ET-1-induced cardiomyocyte hypertrophy and whether the Pin1 inactivation contributes to the inhibitory effect of statins. The aim of this study was to reveal these questions.