Crosstalk between stress and cytokine signaling in metabolic syndrome

在本研究中，我们利用脂肪细胞、肝细胞和胰腺β细胞检查了代谢综合征中应激和炎症细胞因子信号传导之间的串扰，特别关注由各种应激诱导的假激酶家族TRB成员的贡献。这两种信号均强烈减弱脂肪细胞（3T3-L1细胞和HW11细胞）的成熟和功能。另一方面，在人肝癌细胞系 HepG2 细胞中，应激诱导的 TRB3 有效抑制炎症细胞因子之一 TGFβ 的信号传导。此外，由内质网应激诱导的β细胞系Min6细胞的损伤可以被TGFβ挽救。我们的研究结果表明，两种信号的串扰显示了细胞特异性表型，并且 TRB 蛋白起到了这些反应的调节器的作用。

In this study, we examined the crosstalk between stress and inflammatory cytokine signaling in metabolic syndrome using adipocytes, hepatocytes and pancreatic beta cells, especially focused on contribution of the members of pseudokinase family TRBs, which are induced by various stresses.Both signals were strongly attenuated the maturation and function of adipocytes(3T3-L1 cells and HW11 cells). On the other hand, in human hepatoma cell line, HepG2 cells, stress induced TRB3 potently inhibited the signaling of one of the inflammatory cytokines, TGFβ. Moreover the impairment ofβcell line, Min6 cells, induced by endoplasmic reticulum stress is rescued by TGFβ. Our findings suggest that the crosstalk of both signal showed the cell-specific phenotype, and that TRBs proteins function as the tuner of these responses.