Cyclooxygenase-2 induction by adiponectin is regulated by a sphingosine kinase-1 dependent mechanism in cardiac myocytes

被引:54
作者
Ikeda, Yasumasa [1 ]
Ohashi, Koji [1 ]
Shibata, Rei [1 ,2 ]
Pimentel, David R. [3 ,4 ]
Kihara, Shinji [5 ]
Ouchi, Noriyuki [1 ]
Walsh, Kenneth [1 ]
机构
[1] Boston Univ, Sch Med, Mol Cardiol Whitaker Cardiovasc Inst, Boston, MA 02118 USA
[2] Nagoya Univ, Grad Sch Med, Dept Cardiol, Showa Ku, Nagoya, Aichi 4668550, Japan
[3] Boston Univ, Med Ctr, Dept Med, Cardiovasc Med Sect, Boston, MA 02118 USA
[4] Boston Univ, Sch Med, Myocardial Biol Unit, Boston, MA 02118 USA
[5] Osaka Univ, Grad Sch Med, Dept Metab Med, Suita, Osaka 5650871, Japan
来源
FEBS LETTERS | 2008年 / 582卷 / 07期
关键词
adiponectin; cyclooxygenase-2; sphingosine kinase-1; cardiac myocytes;
D O I
10.1016/j.febslet.2008.03.002
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
The adipose-derived plasma protein, adiponectin (APN), has various protective effects on cardiovascular diseases. In this study, we show that endogenous APN is required for full cyclooxygenase-2 (COX-2) induction by ischemia-reperfusion injury in the heart in vivo. In rat neonatal cardiac myocytes, APN-induced COX-2 expression was reduced by treatment with a sphingosine kinase-1 (SphK-1) inhibitor or siRNA targeting SphK-1. Treatment with a sphingosine-1-phosphate (S1P) receptor antagonist also diminished COX-2 expression in response to APN stimulation. These findings suggest that APN is a physiological regulator of COX-2 signaling in the heart and that this regulation occurs in part via a SphK-1-S1P receptor dependent mechanism in cardiac myocytes. (C) 2008 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.
引用
收藏
页码:1147 / 1150
页数:4
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