Polyinosinic-polycytidylic acid inhibits the differentiation of mouse preadipocytes through pattern recognition receptor-mediated secretion of tumor necrosis factor-α.
作者： Lili Yu , Guoyan Liu , Can Yang , Xiangfeng Song , Hui Wang
DOI: 10.1038/ICB.2016.57
关键词:
摘要: Viral infections can disturb the functions of adipose tissues and thus result in metabolic diseases. Polyinosinic-polycytidylic acid (poly(I:C)), a synthetic analog viral double-stranded RNA, induces innate antiviral responses by mimicking infection through activation pattern recognition receptors (PRRs) such as Toll-like receptor 3 (TLR3), retinoic acid-inducible gene I (RIG-I) melanoma differentiation-associated 5 (MDA5). Poly(I:C) also inhibits differentiation mouse preadipocytes but mechanism underlying this process remains unclear. In study, poly(I:C) inhibited preadipocyte dose-dependent manner, not time-dependent manner. Endogenously transfected severely impaired adipogenesis compared with exogenously added poly(I:C). Low concentration tumor necrosis factor-α (TNF-α) could effectively inhibit differentiation. The effect on inhibition was significantly diminished TLR3 knockout mice. By contrast, endogenously still TLR3-deficient preadipocytes. Hence, MDA5/RIG-I signaling involved poly(I:C)-induced stimulation, either endogenous transfection or exogenous addition, TNF-α These results confirmed evidence that PRR-mediated secretion TNF-α.
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