CD44 promotes angiogenesis in myocardial infarction through regulating plasma exosome uptake and further enhancing FGFR2 signaling transduction

• DOI: 10.1186/s10020-022-00575-5
• Publication Date: 2022-12-03T06:03:21Z
• Authors: Qing Zhang; Li Chen; Liyi Huang; Hongxin Cheng; Lu Wang; Lin Xu; Danrong Hu; Chengqi He; Chenying Fu; Quan Wei
• Keywords: Exosome; Knockout mouse

Abstract Background Since angiogenesis occurs as the pathological process following myocardial infarction to alleviate ischemia, therapeutic has been proposed be a cardioprotective strategy. CD44 implicated in endothelial cell functions and its role well established for years. Although recent studies indicate close correlation between exosome, two being ischemia processes, effect underlying mechanism of regulated plasma exosome post-myocardial have not fully elucidated. Methods In this study, we used knockout mice study vivo impacts on ischemic infarction. Mouse cardiac function was measured by echocardiography, histological changes were observed Evans Blue TTC-double staining Masson’s trichrome staining, molecular detected immunofluorescence. vitro HUVECs generated inhibitor angiogenesis. We performed immunoprecipitation, proximity ligation assay, super-resolution imaging mechanistic regulation FGFR2 signaling transduction CD44. Importantly, also isolated exosomes from model studied activation pathway related phenotypic alterations, including uptake angiogenic primary mouse microvascular cells, further discovered exosomal miRNAs. Results that expression border zone infarcted heart tightly ischemia. The depletion impaired biogenesis proangiogenic exosomes. Subsequently, found mediated caveolin 1-dependent vascular cells. Most importantly, miRNAs depended upon participation CD44/FGFR2 Conclusion crucial potent activity. Our elucidate plays key miRNA-enhanced singling early stage