Open Access Peer-reviewed Research Article

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

Main Article Content

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

Abstract

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.

Keywords
heat stress, porcine macrophages, suppressor of cytokine signaling, nuclear factor-κB, MyD88-adapter-like protein

Article Details

How to Cite
Yong, Y., Wu, L., Ma, M., Fang, B., Yu, T., Li, J., Hu, C., Jia, R., & Ju, X. (2019). SOCS1/2 controls NF-κB activity induced by HSP70 by degrading MyD88-adapter-like protein (Mal) in porcine macrophages. Frontiers in Molecular Immunology, 1(1), 3-12. https://doi.org/10.25082/FMI.2019.01.001

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