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- W1513876871 abstract "In type 1 diabetes (T1D), an autoimmune insulitis leads to β-cell death. The non-obese diabetic (NOD) mouse model mimics these facets of the human disease. Our laboratory has previously shown that mice deficient in the alpha subunit of the heterotrimeric G protein, Gz (Gαz), were protected from developing chemically induced diabetes via decreased β-cell apoptosis and increased replication. We aimed to confirm this in the NOD model, as well as delineate the mechanisms of any protection. Between 4-16 weeks of age, weekly blood glucose levels were monitored in wild-type and Gαz-null NOD mice. As compared to wild-type mice, Gαz-null mice were completely protected from developing hyperglycemia. Pancreas histologic analysis showed that Gαz-null pancreata had significantly lower insulitis scores at 16 weeks as compared to wild-type mice. We hypothesized that decreased immune infiltration increased β-cell survival. To test our hypothesis, we calculated beta-cell fractional area, and found it was increased in Gαz-null NOD mice. New cohorts of mice were sacrificed at 4, 8, and 12 weeks of age. At 4 weeks, immune infiltration was already observed in the wild-type islets, correlating with apoptotic beta-cells in islet regions immediately surrounding the invading immune cells. As the first step in delineating mechanism, we showed that islets from Gαz-null NOD mice have significantly less IL-1β and IL-6 cytokine expression; pro-inflammatory cytokines that have been linked with β-cell death. Overall, our results further strengthen our claim that Gαz has a protective effect in maintaining β-cell regeneration and survival, and that the Gαz signaling pathway may be a valid therapeutic target for T1D." @default.
- W1513876871 created "2016-06-24" @default.
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- W1513876871 date "2015-04-01" @default.
- W1513876871 modified "2023-09-26" @default.
- W1513876871 title "The Inhibitory G‐protein, G z , Accelerates the Progression of Insulitis and Hyperglycemia in a Type 1 Diabetes Mouse Model" @default.
- W1513876871 doi "https://doi.org/10.1096/fasebj.29.1_supplement.973.1" @default.
- W1513876871 hasPublicationYear "2015" @default.
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