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Matrix metalloproteinase-28 deletion exacerbates cardiac dysfunction and rupture after myocardial infarction in mice by inhibiting M2 macrophage activation Ma Y; Halade GV; Zhang J; Ramirez TA; Levin D; Voorhees A; Jin YF; Han HC; Manicone AM; Lindsey MLCirc Res 2013[Feb]; 112 (4): 675-88RATIONALE: Matrix metalloproteinase (MMP)-28 regulates the inflammatory and extracellular matrix responses in cardiac aging, but the roles of MMP-28 after myocardial infarction (MI) have not been explored. OBJECTIVE: To determine the impact of MMP-28 deletion on post-MI remodeling of the left ventricle (LV). METHODS AND RESULTS: Adult C57BL/6J wild-type (n=76) and MMP null (MMP-28((-/-)), n=86) mice of both sexes were subjected to permanent coronary artery ligation to create MI. MMP-28 expression decreased post-MI, and its cell source shifted from myocytes to macrophages. MMP-28 deletion increased day 7 mortality because of increased cardiac rupture post-MI. MMP-28(-/-) mice exhibited larger LV volumes, worse LV dysfunction, a worse LV remodeling index, and increased lung edema. Plasma MMP-9 levels were unchanged in the MMP-28((-/-)) mice but increased in wild-type mice at day 7 post-MI. The mRNA levels of inflammatory and extracellular matrix proteins were attenuated in the infarct regions of MMP-28(-/-) mice, indicating reduced inflammatory and extracellular matrix responses. M2 macrophage activation was impaired when MMP-28 was absent. MMP-28 deletion also led to decreased collagen deposition and fewer myofibroblasts. Collagen cross-linking was impaired as a result of decreased expression and activation of lysyl oxidase in the infarcts of MMP-28(-/-) mice. The LV tensile strength at day 3 post-MI, however, was similar between the 2 genotypes. CONCLUSIONS: MMP-28 deletion aggravated MI-induced LV dysfunction and rupture as a result of defective inflammatory response and scar formation by suppressing M2 macrophage activation.|Animals[MESH]|Cell Adhesion Molecules/biosynthesis/genetics[MESH]|Cicatrix/enzymology/etiology[MESH]|Collagen/metabolism[MESH]|Cytokines/biosynthesis/genetics[MESH]|Extracellular Matrix Proteins/biosynthesis/genetics[MESH]|Female[MESH]|Gene Expression Regulation[MESH]|Heart Rupture/*enzymology/etiology[MESH]|Inflammation[MESH]|Macrophage Activation/*physiology[MESH]|Macrophages/classification/enzymology[MESH]|Male[MESH]|Matrix Metalloproteinase 9/blood[MESH]|Matrix Metalloproteinases, Secreted/*deficiency/genetics/physiology[MESH]|Mice[MESH]|Mice, Inbred C57BL[MESH]|Mice, Knockout[MESH]|Myocardial Infarction/blood/complications/*enzymology/physiopathology[MESH]|Myocytes, Cardiac/enzymology[MESH]|Myofibroblasts/metabolism[MESH]|Protein-Lysine 6-Oxidase/metabolism[MESH]|Pulmonary Edema/enzymology/etiology[MESH]|Receptors, Cytokine/biosynthesis/genetics[MESH]|Transcription, Genetic[MESH]|Ventricular Dysfunction, Left/*enzymology/etiology[MESH]|Ventricular Remodeling/genetics/physiology[MESH] |
