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. 2021 Aug 11;9:693342. doi: 10.3389/fcell.2021.693342

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Copyright © 2021 Hu, Li, Wang, Chen, Qian and Dai.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Triggering receptor expressed on myeloid cells 2 (TREM2) silencing modulates microglial polarization at 12 h after subarachnoid hemorrhage (SAH). (A) Higher-magnification images showed the morphological change of primary microglia in vitro. (B,C) Immunofluorescence staining and quantitative analysis of the knockdown efficiency of TREM2 in vitro. (D–I) Representative Western blot bands and quantification of TREM2, soluble TREM2, TREM2 mRNA, ionized calcium-binding adaptor molecule 1(Iba1), cleaved caspase-3, and β-actin. (J–N) Quantitative real-time PCR detection revealed the relative mRNA levels of M2 phenotype mRNA [interleukin (IL)-10], M1 phenotype mRNA [tumor necrosis factor (TNF)α and IL-1β], phagocytic gene (Axl), and lipid metabolism-related gene (Lpl). (O) The changes of microglial viabilities were determined by TREM2 knockdown. These data are shown as mean ± SEM (*p<0.05, **p<0.01, ***p<0.001, ****p<0.001; scale bar = 50 μm).