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Myocardial infarction (MI) results in necrosis, inflammation and scar formation in the myocardium. Such pathological insults place increasing mechanical demands on surviving cardiomyocytes (Boudoulas & Hatzopoulos, 2009). As cardiomyocytes have limited regenerative potential, loss of functional healthy tissue and subsequent left ventricular (LV) remodelling, eventually leads to pathological hypertrophic cardiomyopathy. Hypertrophy of the LV has been documented as a chronic response to MI and invariably progresses to heart failure (Hannigan et al., 2007). Chronic heart failure is a major health problem with patients experiencing a debilitating quality of life. Cardiac remodelling after MI is characterised by progressive and pathological interstitial fibrosis. During acute phase of cardiac repair, degradation of myocardial extracellular matrix (ECM) coupled with an influx of inflammatory cells and cytokines permits deposition of granulation tissue in the infarct region. At the site of tissue injury, granulation tissue composes of macrophages, myofibroblasts and neovascularisation. Activated myofibroblasts synthesise collagen and other ECM proteins to form dense scar tissue in the infarct in response to inflammatory mediators such as angiotensin II (Ang II) and transforming growth factor-1 (TGF-1). Macrophages drive the production of TGF1, an essential growth factor for fibroblast production, collagen synthesis and inhibition of collagen degradation (O'Kane & Ferguson, 1997; Sun & Weber, 2000). At the site of MI, increased expression of adhesion molecules (inter-cellular adhesion molecule-1, ICAM-1) and chemoattractant cytokines (monocyte chemotactic protein-1, MCP-1) facilitate migration of inflammatory cells (e.g. macrophages) enabling scavenging of necrotic tissues (Lu et al., 2004). This couples with elevated expression of matrix metalloproteinase-1 (MMP-1) results in remodelling of myocardial ECM by degradation of existing collagen I and III in the injured myocardium (Lu et al., 2004). Furthermore, MMP-9 has been implicated in tissue remodelling by cleaving collagen V at the aminoterminus (Niyibizi et al., 1994). Consequently, this process compromises structural integrity of the ventricles, resulting in myocyte slippage, wall thinning and rupture

Dynamic Relationships of Collagen Extracellular Matrices on Cardiac Differentiation of Human Mesenchymal Stem Cells