Interleukin-27 Protects Cardiomyocyte-Like H9c2 Cells against Metabolic Syndrome: Role of STAT3 Signaling.

Wei-Lian Phan,Ming-Chieh Ma,Yu-Tzu Huang

doi:10.1155/2015/689614

Abstract

The present results demonstrated that high glucose (G), salt (S), and cholesterol C (either alone or in combination), as mimicking extracellular changes in metabolic syndrome, damage cardiomyocyte-like H9c2 cells and reduce their viability in a time-dependent manner. However, the effects were greatest when cells were exposed to all three agents (GSC). The mRNA of glycoprotein (gp) 130 and WSX-1, both components of the interleukin (IL)-27 receptor, were present in H9c2 cells. Although mRNA expression was not affected by exogenous treatment with IL-27, the expression of gp130 mRNA (but not that of WSX-1 mRNA) was attenuated by GSC. Treatment of IL-27 to H9c2 cells increased activation of signal transducer and activator of transcription 3 (STAT3) and protected cells from GSC-induced cytochrome c release and cell damage. The protective effects of IL-27 were abrogated by the STAT3 inhibitor, stattic. The results of the present study clearly demonstrate that the STAT3 pathway triggered by anti-inflammatory IL-27 plays a role in protecting cardiomyocytes against GSC-mediated damage.

Highlights

In humans, metabolic syndrome (MS) is characterized by a combination of obesity, hyperglycemia, glucose intolerance, dyslipidemia, and hypertension [1]
The results of the present study show that the IL-27/signal transducer and activator of transcription 3 (STAT3) pathway plays a role in protecting cardiomyocytes against GSC-mediated damage
We showed that G, S, and C damage H9c2 cells and reduce their viability; the effects were greatest when cells were exposed to all three agents (GSC)

Summary

Introduction

Metabolic syndrome (MS) is characterized by a combination of obesity, hyperglycemia, glucose intolerance, dyslipidemia, and hypertension [1]. The risk of heart attack is three times greater for those with MS than for those without [2]. MS renders the myocardium intolerant to further injury, including ischemia or mechanical damage. This notion is supported by a recent study showing that MS increases apoptosis in rat cardiomyocytes after myocardial ischemia/reperfusion (IR) injury via reactive oxygen species- (ROS-) mediated increases in mitochondrial permeability [6]. It is necessary to explore the mechanism underlying the effects of MS on the myocardium with a view on developing new treatments for heart diseases associated with metabolic disorders

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