Biochemical and biophysical research communications · 2013
Midkine exacerbates pressure overload-induced cardiac remodeling.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
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Netsu Shunsuke, Shishido Tetsuro, Kitahara Tatsuro, Honda Yuki, Funayama Akira, Narumi Taro, Kadowaki Shinpei, Takahashi Hiroki, Miyamoto Takuya, Arimoto Takanori, Nishiyama Satoshi, Watanabe Tetsu, Woo Chang-Hoon, Takeishi Yasuchika, Kubota Isao
Аннотация
Midkine is a multifunctional growth factor, and its serum levels are increased with the functional severity of heart failure. This study aimed to examine the role of midkine in heart failure pathogenesis. Midkine expression levels were increased in the kidney and lung after transverse aortic constriction (TAC) surgery, but not sufficiently increased in the heart. After TAC, phosphorylation of extracellular signal-regulated kinase1/2 and AKT, and the expression levels of foetal genes in the heart were considerably increased in transgenic mice with cardiac-specific overexpression of midkine (MK-Tg) compared with wild-type (WT) mice. MK-Tg mice showed more severe cardiac hypertrophy and dysfunction, and showed lower survival rate after TAC than WT mice. We conclude that midkine plays a critical role in cardiac hypertrophy and remodelling.