Toll-like Receptor 4 Mediates the Inflammatory Responses and Matrix Protein Remodeling in Remote Non-Ischemic Myocardium in a Mouse Model of Myocardial Ischemia and Reperfusion

摘要: The signaling mechanism that mediates inflammatory responses in remote non-ischemic myocardium following regional ischemia/reperfusion (I/R) remains incompletely understood. Myocardial Toll-like receptor 4 (TLR4) can be activated by multiple proteins released from injured cells and plays a role myocardial inflammation injury expansion. We tested the hypothesis TLR4 occupies an important mediating matrix protein remodeling I/R injury. Methods results: TLR4-defective (C3H/HeJ) TLR4-competent (C3H/HeN) mice were subjected to coronary artery ligation (30 min) reperfusion for 1, 3, 7 or 14 days. In mice, levels of monocyte chemoattractant -1 (MCP-1), keratinocyte (KC), intercellular adhesion molecule 1 (ICAM-1) vascular cell (VCAM-1) elevated at day reperfusion. Levels collagen I, IV, metalloproteinase (MMP) 2 MMP 9 increased activities also increased. deficiency resulted moderate reduction infarct size. However, it markedly downgraded changes chemokines, molecules myocardium. Further, left ventricular function was significantly improved mice. conclusion, contributes adverse cardiac remodeling.