The ability to suppress macrophage-mediated inflammation in orbital fat stem cells is controlled by miR-671-5p

Lien, Gi-Shih; Liu, Jen-Fang; Chien, Ming-Hsien; Hsu, Wei-Tse; Chang, Tzu-Hao; Ku, Chia-Chi; Ji, Andrea Tung-Qian; Tan, Peng; Hsieh, Ting-Lieh; Lee, Liang-Ming; Ho, Jennifer H

Recently, miRNAs have been identified as critical regulators of immune responses [44, 45] , and LPS stimulation may alter the expression of miRNAs in macrophages [46] [47] [48] . MiR-155 is upregulated in LPS-activated macrophages in response to TNFα interrupting macrophage differentiation and toll-like receptor 4 transcription [47] [48] [49] . In contrast, miR-125b is downregulated in LPS-treated macrophages for inhibiting TNFα expression [48] . However, we disclosed that miR-671-5p in MSCs derived from orbital fat tissues played a role in regulation of IL-1RA and sTNFR type II. Although miR-671-5p was predicted to interact with IL-10, IL-1RA and sTNFR type II (Table 1) , only sTNFR type II and IL-1RA were directly inhibited by miR-671-5p ( Figure 5B,C,D) . Reduction of miR-671-5p in OFSCs in a macrophage-mediated proinflammatory environment ( Figure 5A ) resulted in the upregulation of sTNFR type II and IL-1RA in OFSCs ( Figures 4D,E and 5B) , which contributed to the anti-inflammation ability of OFSCs in vivo ( Figure 6D ).