SOCS3 control the activity of NF-jB induced by HSP70 via degradation of MyD88-adapter-like protein (Mal) in IPEC-J2 cells
SOCS3 control the activity of NF-jB induced by HSP70 via degradation of MyD88-adapter-like protein (Mal) in IPEC-J2 cells
复制标题
SOCS3 通过降解 IPEC-J2 细胞中的 MyD88 适配器样蛋白 (Mal) 控制 HSP70 诱导的 NF-jB 活性
DOI：
10.1080/02656736.2018.1541484
复制
发表时间：
2018
影响因子：
3.1
通讯作者：
Xiang-Hong Ju
中科院分区：
文献类型：
--
作者：
Yan-Hong Yong;Ping Wang;Ru-Min Jia;Ravi Gooneratne;Hwa-Chain Robert Wang;Ming Liao;Xiang-Hong Ju
Hyperthermia in pigs induces suppressor of cytokine signaling (SOCS) 3 and SOCS4 expression in intestinal gut and causes disruption of inflammation cytokine production. These changes may affect the development of inflammatory bowel disease in heat-stressed pigs. However, the mechanisms are not well understood. Accordingly, in this study, we examined the roles of SOCS members in regulation of the nuclear factor (NF)-κB pathway and heat shock protein (HSP) 70-mediated cytokine induction in 293T human embryonic kidney cells and IPEC-J2 porcine small intestinal epithelial cells. Ectopic expression of HSP70 significantly modulated NF-κB activity (p≤ .05). Moreover, co-expression of SOCS3 or SOCS4 with HSP70 reduced NF-κB activity, which was abolished by SOCS3 or SOCS4 knockdown with short hairpin RNA. Interestingly, MyD88-adaptor-like (Mal) protein was downregulated in cells expressing SOCS3 but not in cells expressing SOCS4. In addition, SOCS3 but not SOCS4 negatively regulated the activity of NF-κB induced by HSP70 overexpressionviadegradation of Mal. These findings may facilitate the development of novel SOCS3-based therapeutic strategies to control heat stress-related disorders in pigs.
