Midkine exacerbates pressure overload-induced cardiac remodeling

被引：24

作者：

Netsu, Shunsuke ^{[1
]}

Shishido, Tetsuro ^{[1
]}

Kitahara, Tatsuro ^{[1
]}

Honda, Yuki ^{[1
]}

Funayama, Akira ^{[1
]}

Narumi, Taro ^{[1
]}

Kadowaki, Shinpei ^{[1
]}

Takahashi, Hiroki ^{[1
]}

Miyamoto, Takuya ^{[1
]}

Arimoto, Takanori ^{[1
]}

Nishiyama, Satoshi ^{[1
]}

Watanabe, Tetsu ^{[1
]}

Woo, Chang-Hoon ^{[2
]}

Takeishi, Yasuchika ^{[3
]}

Kubota, Isao ^{[1
]}

机构：

[1] Yamagata Univ, Sch Med, Dept Cardiol Pulmonol & Nephrol, Yamagata 9909585, Japan

[2] Yeungnam Univ, Coll Med, Dept Pharmacol, Taegu, South Korea

[3] Fukushima Med Univ, Dept Cardiol & Hematol, Fukushima, Japan

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2014年 / 443卷 / 01期

基金：

日本学术振兴会;

关键词：

Midkine; Heart failure; Cardio-renal interaction; CHRONIC HEART-FAILURE; MYOCARDIAL-INFARCTION; HYPERTROPHY; DYSFUNCTION; PREVENTS; MICE; INFLAMMATION; INJURY; PLEIOTROPHIN; ASSOCIATION;

D O I：

10.1016/j.bbrc.2013.11.083

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

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. (C) 2013 The Authors. Published by Elsevier Inc. All rights reserved.

引用

页码：205 / 210

页数：6

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