期刊
INTERNATIONAL JOURNAL OF HYPERTHERMIA
卷 36, 期 1, 页码 151-159出版社
TAYLOR & FRANCIS LTD
DOI: 10.1080/02656736.2018.1541484
关键词
Heat stress; IPEC-J2 cells; suppressor of cytokine signaling 3; nuclear factor-kappa B; MyD88-adapter-like protein
资金
- National Natural Science Foundation of China [31101862, 31472243]
- Shenzheng Projects for Basic Research [JCYJ2017030616241 4058]
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)-kappa B 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-kappa B activity (p <= .05). Moreover, co-expression of SOCS3 or SOCS4 with HSP70 reduced NF-kappa B 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-kappa B induced by HSP70 overexpression via degradation of Mal. These findings may facilitate the development of novel SOCS3-based therapeutic strategies to control heat stress-related disorders in pigs.
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