Exosomes derived from M1 macrophages aggravate neointimal hyperplasia following carotid artery injuries in mice through miR-222/CDKN1B/CDKN1C pathway

• DOI: 10.1038/s41419-019-1667-1
• Publication Date: 2019-05-29T13:03:06Z
• Authors: Zeng Wang; Hong Zhu; Hongtao Shi; Huan Zhao; Rifeng Gao; Xinyu Weng; Rongle Liu; Xiao Li; Yunzeng Zou; Kai Hu; Aijun Sun; Junbo Ge
• Keywords: Neointimal hyperplasia; Neointima

Abstract The role of M1 macrophages (M1M)-derived exosomes in the progression neointimal hyperplasia remains unclear now. Using a transwell co-culture system, we demonstrated that M1M contributed to functional change vascular smooth muscle cell (VSMC). We further stimulated VSMCs with isolated from M1M. Our results these could be taken up by through macropinocytosis. microRNA array assay, identified miR-222 originated M1M-derived triggered changes VSMCs. In addition, confirmed played key promoting proliferation and migration targeting Cyclin Dependent Kinase Inhibitor 1B (CDKN1B) 1C (CDKN1C) vitro. vivo, significantly aggravated neointima formation following carotid artery ligation injury wire effects were partly abolished inhibitor 2′OMe-miR-222. findings thus suggest derived aggravate delivering into Future studies are warranted validate if post-injury restenosis attenuated inhibiting miR-222.