Key result
Administration of M2b macrophages improved survival, left ventricular systolic function, and alleviated myocardial fibrosis compared to vehicle in a rat model of ischemia/reperfusion injury.
Why the study?
M2b macrophages modulate inflammatory immune responses without participating in wound healing, leading to the hypothesis that they could improve cardiac function and ameliorate fibrosis after myocardial ischemia/reperfusion injury.
Administration of M2b macrophages attenuates myocardial remodeling after ischemia/reperfusion injury in rats, potentially by regulating PDGFR kinase activation in cardiac fibroblasts.
Not ready to inform post-MI care; leaves open translation of M2b macrophage benefits to human remodeling.
Background: Myocardial injury is a major cause of myocardial remodeling. Macrophages are important in cardiac repair as a result of their interactions with fibroblasts. As regulatory macrophages, M2b macrophages modulate inflammatory immune responses without participating in wound healing and could have enhanced protective effects on myocardial remodeling. Therefore, we tested the hypothesis that M2b macrophages could improve cardiac function and ameliorate myocardial fibrosis after the myocardial ischemia/reperfusion injury (MI/RI). Methods: In vivo, MI/RI models were established with Sprague-Dawley (SD) rats and either M2b macrophages (MT group) or the same volume of vehicle (CK group) was injected into the ischemic zone. Two weeks after the operation, cardiac function and diameters were determined by echocardiography examination. Level of myocardial fibrosis was measured by Sirius red staining and the expression of fibrosis-related factors. In vitro, cardiac fibroblasts (CFs) were co-cultured with M2b macrophages or cultured with M2b macrophage supernatant. Expression of α-smooth muscle actin (α-SMA) and connective tissue growth factor (CCN2/CTGF) in the CFs were measured by western blotting and immunofluorescence staining. In addition, the expression of platelet-derived growth factors (PDGFs), the expression of platelet-derived growth factor receptors (PDGFRs) and the phosphorylation of PDGFRs was detected by western blotting. Results: A significantly higher rat survival rate, improved left ventricular (LV) systolic function, decreased diameter of the LV and alleviated myocardial fibrosis were observed in the MT group than in the CK group. In vitro, the activation of CFs was significantly reduced by the M2b macrophages treatments, relative to the blank control. In addition, the kinase activation of PDGFRs was decreased by M2b macrophage treatments both in vivo and in vitro. Conclusions: Our study demonstrated that the administration of M2b macrophages could attenuate myocardial remodeling after MI/RI. The regulation of the activation of PDGFRs in CFs is an important part of the protective mechanism.
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Yuan et al. (2020) studied Myocardial ischemia/reperfusion injury. M2b macrophages vs. Vehicle was evaluated on Rat survival rate, left ventricular systolic function, left ventricular diameter, and myocardial fibrosis. Administration of M2b macrophages improved survival, left ventricular systolic function, and alleviated myocardial fibrosis compared to vehicle in a rat model of ischemia/reperfusion injury.
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