MicroRNA-101a regulates microglial morphology and inflammation

Background: microglia,as well as other tissue-resident macrophages,arise from yolk sac progenitors. thus,it is likely that the central nervous system environment is critical for the acquisition of a distinct microglial phenotype. several micrornas that are enriched in the brain play crucial roles in brain development and may also play a role in the differentiation of microglia. methods: to track the differentiation of hematopoietic cells into microglia,lineage-negative bone marrow cells were co-cultured with astrocytes in the absence or presence of micrornas or their inhibitors. microglia-like cells were identified as small,round cells that were immunopositive for cd11b,iba1,cx3cr1,and triggering receptor expressed on myeloid cells (trem)-2. results: five micrornas (mir-101a,mir-139-3p,mir-214*,mir-218,and mir-1186) were identified as modifiers of the differentiation of bone marrow-derived microglia-like cells. among them,mir-101a facilitated the differentiation of bone marrow cells into microglia-like cells most potently. small,round cells expressing cd11b,iba1,cx3cr1,and trem-2 were predominant in cells treated by mir-101a. mir-101a was abundantly expressed in non-microglial brain cells. transfection of mir-101a into microglia significantly increased the production of il-6 in response to lps. finally,mir-101a downregulated the expression of mapk phosphatase-1. conclusions: mir-101a,which is enriched in the brain,promotes the differentiation of bone marrow cells into microglia-like cells. © 2017 the author(s).