Role of matricellular proteins in cardiac tissue remodeling after myocardial infarction

Table 1 Expression of matricellular proteins and phenotypes of matricellular gene null mice after MI

Protein	Expression after MI	Phenotypes of matricellular gene null mice after MI as compared with WT mice	Heart functionafter MI	Possible mechanism responsible for phenotypes of gene null mice after MI	Ref.
OPN	↑ Early and late phases	Increase in LV dilation with reduced collagen synthesis and accumulation in the infarct as well as non-infarct regions	↓	Macrophage recruitment and phagocytosis ↓	[17,18]
	Macrophages and fibroblasts			Fibroblast adhesion and proliferation ↓
				Myofibroblast differentiation ↓
				ECM deposition ↓
TSP-1	↑ Early phase	More inflammation and expansion of the infarct and enhanced ventricular dilatation	ND	Inflammation ↑	[19]
	Inflammatory cells			TGF-β1 signaling ↓
				MMP-9 activity ↑
TSP-2	↑ Late phase	Increased incidence of cardiac rupture	ND	Maturation of the infarct scar ↓	[20]
	Fibroblasts			MMP activity ↑
TNC	↑ Early phase	Reduced end-diastolic pressure and LV dimension with less interstitial fibrosis	↑	De-adhesion ↓	[21]
	Fibroblasts			MMPs production ↓
				Fibrosis ↓
TNX	ND	ND	ND	ND	ND
Periostin	↑ Early and late phases	Increased incidence of cardiac rupture with decreased recruitment of myofibroblasts and impaired collagen fiber formation in the infarct	↑	Integrity of the ECM ↓	[22,23]
	Fibroblasts			Adhesion-dependent signaling ↓
SPARC	↑ Early and late phases	Increased incidence of cardiac rupture with disorganized granulation tissue and immature collagenous ECM	↓	Collagen matrix maturation ↓	[24]
	Myofibroblasts and leucocytes			TGF-β1 signaling ↓

MI: Myocardial infarction; WT: Wild-type; OPN: Osteopontin; LV: Left ventricle; ECM: Extracellular matrix; TSP: Thrombospondin; ND: Not determined; TGF-β1: Transforming growth factor-β1; MMP: Matrix metalloproteinase; TNC: Tenascin-C; TNX: Tenascin-X; SPARC: Secreted protein, acid and rich in cysteine; also known as osteonectin.