Midkine exacerbates pressure overload-induced cardiac remodeling |
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| Authors: | 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 |
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| Affiliation: | 1. Department of Cardiology, Pulmonology, and Nephrology, Yamagata University School of Medicine, Yamagata, Japan;2. Department of Pharmacology, College of Medicine, Yeungnam University, Daegu, Republic of Korea;3. Department of Cardiology and Hematology, Fukushima Medical University, Fukushima, Japan |
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| Abstract: | 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. |
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| Keywords: | 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 |
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