Background: When the multicystic vesicles (precursor of exosomes) are formed in cells, there are two results. One is to be decomposed by lysosomes and the other one is to become exosomes which are transported out through transmembrane. On the other hand, M2 macrophages can promote the formation of local vascularization and provide necessary support for the repair of bone defects. In order to provide a new idea for the treatment of bone defects, the purpose of our study is to investigate the effect of WKYMVm peptide on the secretion of exosomes from murine bone marrow-derived MSCs (mBMSCs) and the effect of exosomes on the polarization of M2 macrophages. Methods: WKYMVm peptide was used to activate the Formyl Peptide Receptor 2 (FPR2) pathway in mBMSCs. At first, we used CCK-8 kit to detect the cytotoxic effect of WKYMVm Peptide on mBMSCs. Secondly, we used western blotting and Quantitative real-time Polymerase Chain Reaction (Qrt-PCR) to detect the expression of Interferon Stimulated Gene 15 (ISG15) and Transcription Factor EB (TFEB) in mBMSCs. Thirdly, we used exosomes extraction kit and western blotting to detect the content of exosomes secreted by mBMSCs. Finally, we used the immunofluorescence and western blotting to count the number of M2 macrophages polarization.Results: We firstly found that WKYMVm peptide had no toxic effect on mBMSCs at the concentration of 1μmol/L. Secondly, we found that when the FPR2 pathway was activated by WKYMVm peptide in mBMSCs, the expression of ISG15 and TFEB were decreased, leaded to the secretion of exosomes increased. Finally, we proved that the exosomes secreted by mBMSCs could promote the polarization of M2 macrophages. Moreover, all these effects can be blocked by WRWWWW (WRW4) peptide, an inhibitor of FPR2 pathway.Conclusion: Our findings demonstrated the potential value of WKYMVm peptide in promoting the secretion of exosomes by mBMSCs and eventually leading to M2 macrophages polarization. We believed that our study could provide a research basis for the clinical treatment of bone defects.
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