Myocardial expression analysis of osteopontin and its splice variants in patients affected by end-stage idiopathic or ischemic dilated cardiomyopathy

M Cabiati,B Svezia,M Matteucci,L Botta,A Pucci,C Caselli,V Lionetti,S Del Ry

doi:10.1016/j.vph.2015.11.011

Abstract

Myocardial expression analysis of osteopontin and its splice variants in patients affected by end-stage idiopathic or ischemic dilated cardiomyopathy

Highlights

Adverse structural remodelling leads to heart failure (HF) that is characterized by ongoing structural rearrangement in the architecture of the ventricular myocardium resulting in clinical and pathophysiological overt HF [1]
Pre-clinical studies demonstrated that healthy murine myocardium expresses low levels of OPN in response to increased afterload [6] and in human, increased plasma levels of OPN are associated with activation of the renin-aldosterone system and with myocardial and coronary microvascular damage in dilated cardiomyopathy [7] but it is still poorly defined whether its expression changes in failing heart of different origin
In order to understand if OPN and thrombin expression were dependent on the origin of HF rather than the magnitude of global cardiac function, their expression was analyzed in VLP with LVEF>50% and compared with the whole group of failing patients (DCM+ICM) with LVEF

Summary

Introduction

Adverse structural remodelling leads to heart failure (HF) that is characterized by ongoing structural rearrangement in the architecture of the ventricular myocardium resulting in clinical and pathophysiological overt HF [1]. A key regulator of remodelling process in the heart is the ECM that consists of structural and non-structural proteins interacting via specific cell surface receptors or soluble growth factors and cytokines [4]. Osteopontin (OPN) is a typical phosphoglycoprotein of cardiac ECM often overexpressed in the human blood and remodelled myocardium during the development of HF [5]. Pre-clinical studies demonstrated that healthy murine myocardium expresses low levels of OPN in response to increased afterload [6] and in human, increased plasma levels of OPN are associated with activation of the renin-aldosterone system and with myocardial and coronary microvascular damage in dilated cardiomyopathy [7] but it is still poorly defined whether its expression changes in failing heart of different origin

Objectives

Methods

Results

Discussion

Conclusion