Midkine exacerbates pressure overload-induced cardiac remodeling
详细信息 查看全文
- 作者：Shunsuke Netsu ; Tetsuro Shishido ; Tatsuro Kitahara ; Yuki Honda ; Akira Funayama ; Taro Narumi ; Shinpei Kadowaki ; Hiroki Takahashi ; Takuya Miyamoto ; Takanori Arimoto ; Satoshi Nishiyama ; Tetsu Watanabe ; Chang-Hoon Woo ; Yasuchika Takeishi ; Isao Kubota
- 关键词：TAC ; transverse aortic constriction ; ERK ; extracellular signal-regulated kinase ; MHC ; myosin heavy chain ; PI3K ; phosphatidylinositol 3-kinase ; ANP ; atrial natriuretic peptide ; BNP ; brain natriuretic peptide ; CTGF ; connective tissue growth factor ; GAPDH ; glyceraldehyde 3-phosphate dehydrogenase
- 刊名：Biochemical and Biophysical Research Communications
- 出版年：3 January, 2014
- 年：2014
- 卷：443
- 期：1
- 页码：205-210
- 全文大小：826 K
文摘
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.