Vol 1 No 1 (2019)

Published: 2019-08-15

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SOCS1/2 controls NF-κB activity induced by HSP70 by degrading MyD88-adapter-like protein (Mal) in porcine macrophages

blankpage Yanhong Yong, Lianyun Wu, Minglong Ma, Biao Fang, Tianyue Yu, Junyu Li, Canying Hu, Rumin Jia, Xianghong Ju

Heat stress induces suppressor of cytokine signaling (SOCS) 1 and SOCS2 expression in the intestinal gut and disrupts inflammatory cytokine production in pigs. These changes may be important to the development of inflammatory bowel disease in heat-stressed pigs. However, the underlying mechanisms have not yet been completely elucidated. In the present study, we examined the roles of SOCS1 and SOCS2 in regulating the nuclear factor (NF)-κB pathway in CRL-2845 porcine macrophages. Ectopic expression of HSP70 significantly modulated NF-κB activity (p ≤ 0.05). Moreover, co-expression of SOCS1 or SOCS2 with HSP70 reduced NF-κB activity, which was abolished by SOCS1 or SOCS2 knockdown with  small interfering RNA. Additionally, myeloid differentiation factor 88 (MyD88)-adaptor-like (Mal) protein was down-regulated in cells expressing SOCS1 and SOCS2. SOCS1 and SOCS2 were found to negatively regulate the activity of NF-κB induced by HSP70 overexpression by degrading Mal. These findings may facilitate the development of novel SOCS1-based and SOCS2-based therapeutic strategies for controlling heat stress-related disorders in pigs.

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