Abstract

The endoplasmic reticulum (ER) homeostasis plays a pivotal role in cell physiological functions. Various pathological, physiological, or pharmacological stimuli can destroy ER homeostasis and cause an adaptive response noted as ER stress. Meanwhile, ER stress is frequently associated with inflammatory response. GRP78 (Glucose-regulated protein 78) is crucial to maintaining the homeostasis of cells. Nonetheless, the potential mechanisms underlying the impact of GRP78 on ER stress and inflammation remain incompletely elucidated in fish. In the current research, the ER stress and inflammation were induced by Thapsigargin (TG) treatment in large yellow croaker macrophages. Then, the macrophages were incubated with agonist/inhibitor of GRP78 before or after the TG incubation to figure out the effects of GRP78. The results demonstrated that exposure to TG could significantly induce ER stress and inflammation in large yellow croaker macrophages, while the overexpression of GRP78 attenuated the ER stress and inflammation induced by TG. Furthermore, the inhibition of GRP78 further induced the ER stress and inflammation induced by TG. In conclusion, the above results indicated that GRP78 could regulate the ER stress and inflammation induced by TG in large yellow croaker.

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