ArticleAmerican journal of translational research2025
Exendin-4 protects β-cells against interleukin-1β-induced apoptosis via upregulating GMRP-1.
Article in American journal of translational research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
objectiveTo elucidate whether Exendin-4 (Ex-4) protects β cells against interleukin-1β (IL-1β)-induced apoptosis by regulating glucose metabolism-related protein-1 (GMRP-1) and suppressing the Jun N-terminal kinase (JNK) signaling pathway.
methodsPancreatic β cells were treated with Ex-4 either in the presence or absence of IL-1β. Alterations in the expression of GMRP-1 and JNK signaling pathway-related proteins were examined by quantitative PCR, western blotting, and immunofluorescence. The anti-apoptotic efficacy of Ex-4 against IL-1β-induced apoptosis was assessed using flow cytometry.
resultsEx-4 inhibited IL-1β-induced activation of the JNK pathway and subsequent β-cell apoptosis. This inhibitory effect was associated with the upregulation of the level of GMRP-1. Mechanistically, Ex-4 upregulated GMRP-1 expression in a time- and dose-dependent manner and reversed the IL-1β-induced suppression of GMRP-1. Both
conclusionGMRP-1 serves as an essential mediator of Ex-4's cytoprotective effects. Ex-4 safeguards β cells against IL-1β-induced apoptosis primarily by upregulating GMRP-1, which in turn suppresses the pro-apoptotic JNK pathway. These results provide new insights into the molecular mechanisms underlying diabetes pathogenesis and identify GMRP-1 as a potential therapeutic target for the treatment of diabetes.
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