Exosomes derived from mesenchymal stem cells inhibit neointimal hyperplasia by activating the Erk1/2 signalling pathway in rats

• DOI: 10.1186/s13287-020-01676-w
• Publication Date: 2020-06-08T09:05:57Z
• Authors: Zhihui Liu; Chao Wu; Xinliang Zou; Weiming Shen; Jiacai Yang; Xiaorong Zhang; Xiaohong Hu; Haidong Wang; Yi Liao; Tao Jing
• Keywords: Neointimal hyperplasia; Intimal hyperplasia; Evans Blue; CD31; Immunofluorescence

Restenosis is a serious problem in patients who have undergone percutaneous transluminal angioplasty. Endothelial injury resulting from surgery can lead to endothelial dysfunction and neointimal formation by inducing aberrant proliferation migration of vascular smooth muscle cells. Exosomes secreted mesenchymal stem cells been hot topic cardioprotective research. However, date, exosomes derived (MSC-Exo) rarely reported association with restenosis after artery injury. The aim this study was investigate whether MSC-Exo inhibit hyperplasia rat model carotid balloon-induced and, if so, explore the underlying mechanisms.Characterization immunophenotypes performed electron microscopy, nanoparticle tracking analysis western blot assays. To inhibited hyperplasia, rats were intravenously injected normal saline or Haematoxylin-eosin staining examine intimal media areas. Evans blue dye re-endothelialization. Moreover, immunohistochemistry immunofluorescence expression CD31, vWF α-SMA. further involvement MSC-Exo-induced re-endothelialization, mechanisms studied cell counting kit-8, scratch, assays.Our data showed that ingested systemic injection suppressed results could accelerate re-endothelialization compared group. upregulated CD31 but downregulated Furthermore, mechanistically facilitated activating Erk1/2 signalling pathway. PCNA, Cyclin D1, Vimentin, MMP2 MMP9 control Interestingly, an inhibitor reversed above proteins.Our suggest accelerating which accompanied activation Importantly, our provides novel cell-free approach for treatment diseases intervention.