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- W2116053532 abstract "β-cell apoptosis is a significant contributor to β-cell dysfunction in diabetes and ER stress is among the factors that contributes to β-cell death. We previously identified that the Ca2+-independent phospholipase A2β (iPLA2β), which in islets is localized in β-cells, participates in ER stress-induced β-cell apoptosis. Here, direct assessment of iPLA2β role was made using β-cell-specific iPLA2β overexpressing (RIP-iPLA2β-Tg) and globally iPLA2β-deficient (iPLA2β-KO) mice. Islets from Tg, but not KO, express higher islet iPLA2β and neutral sphingomyelinase, decrease in sphingomyelins, and increase in ceramides, relative to WT group. ER stress induces iPLA2β, ER stress factors, loss of mitochondrial membrane potential (∆Ψ), caspase-3 activation, and β-cell apoptosis in the WT and these are all amplified in the Tg group. Surprisingly, β-cells apoptosis while reduced in the KO is higher than in the WT group. This, however, was not accompanied by greater caspase-3 activation but with larger loss of ∆Ψ, suggest..." @default.
- W2116053532 created "2016-06-24" @default.
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- W2116053532 creator A5075524176 @default.
- W2116053532 creator A5089660671 @default.
- W2116053532 date "2013-01-01" @default.
- W2116053532 modified "2023-10-13" @default.
- W2116053532 title "Genetic modulation of islet β-cell iPLA<sub>2</sub>β expression provides evidence for its impact on β-cell apoptosis and autophagy" @default.
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- W2116053532 doi "https://doi.org/10.4161/isl.23758" @default.
- W2116053532 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3662380" @default.
- W2116053532 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/23411472" @default.
- W2116053532 hasPublicationYear "2013" @default.
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