Why the study?
M1 macrophages inhibit cardiac repair, but their role in myocardial regeneration remains unclear.
M1 macrophage-derived exosomes inhibit cardiomyocyte proliferation and cardiac repair by delivering miR-155, which targets IL-6R and suppresses the IL-6R/Jak/Stat pathway.
M1 macrophages inhibit cardiac repair, but their role in myocardial regeneration remains unclear. In this study, the underlying mechanisms of M1 macrophage-derived exosomes (M1-Exos) in cardiomyocyte proliferation was investigated. Mouse RAW264.7 macrophages were cultured and induced into M1 macrophages. The exosomes from the culture media of M1 macrophages were isolated, and results showed that M1-Exos could inhibit the proliferation of cardiomyocytes. During M1-Exos, miR-155 was highly expressed and delivered to the cardiomyocytes. Furthermore, miR-155 inhibited the proliferation of cardiomyocytes and antagonized the pro-proliferation effect of IL-6 via inhibition of its novel target gene IL-6R. M1-Exos inhibited cardiomyocyte proliferation and cardiac repair by delivering miR-155, which targeted IL-6R, and inhibiting the IL-6R/Jak/Stat signaling pathway. This study provides new insights and potential treatment strategies for the regulation of myocardial regeneration and cardiac repair by M1-Exos.
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He et al. (2022) studied this question.
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