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• W2890530853 abstract "Cyclosporin A (CsA) is widely used as an immunosuppressor in the context of organ transplantation or autoimmune disorders. Recent studies have revealed the detrimental effects of CsA on insulin resistance and pancreatic β cell failure; however, the molecular mechanisms are unknown. The present study sought to confirm the associations between CsA and β cell failure, and to investigate the roles of proinsulin folding and endoplasmic reticulum (ER) stress in CsA-induced β cell failure. The viability of MIN6 cells treated with CsA was evaluated with MTT assay. Expression levels of insulin, peptidyl-prolyl cis-trans isomerase B (PPIB), cleaved caspase-3, phospho-protein kinase R (PKR)-like endoplasmic reticulum kinase (p-PERK), PKR-like endoplasmic reticulum kinase (PERK), binding immunoglobulin protein (BIP), and C/EBP homologous protein (CHOP) were detected via reducing western blot assay. Non-reducing western blot analysis was performed to examine the expression of misfolded proinsulin peptides. The proliferation of MIN6 cells was not inhibited by CsA at concentrations <1 µmol/l. CsA treatment resulted in the decreased expression of insulin and PPIB; however, it also increased the phosphorylation of PERK, and upregulated the expression of PERK, BIP, CHOP and cleaved caspase-3. The results indicated that CsA could induce pancreatic β cell dysfunction and the potential mechanism underlying this phenomenon may be PPIB-associated proinsulin misfolding, which in turn induces ER stress in β cells." @default.
• W2890530853 created "2018-09-27" @default.
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• W2890530853 date "2018-09-07" @default.
• W2890530853 modified "2023-09-28" @default.
• W2890530853 title "Inhibition of peptidyl‑prolyl cis‑trans isomerase B mediates cyclosporin A‑induced apoptosis of islet β cells" @default.
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• W2890530853 doi "https://doi.org/10.3892/etm.2018.6706" @default.
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