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- W198975449 abstract "PTP1B dephosphorylates receptors tyrosine kinase and acts as a brake on various signaling pathways. Deletion of PTP1B protects against metabolic dysfunction by increasing insulin sensitivity, but little is known about its role in the control of vascular function. We hypothesized that PTP1B deletion prevents vascular dysfunction in the absence of insulin. Insulin secretion was abolished in Balb/C and PTP1B-deficient mice with streptozotocin (STZ) injection. 24 days after treatment, aortic reactivity was assessed via myography. STZ induced similar increases in glycemia in Balb/C and PTP1B KO mice (384±24 vs 444±21 mg/dL, Balb/C vs PTP1B). Phenylephrine (PE)-induced constriction was increased by STZ treatment in Balb/C mice only (115±13 vs 136±6% of KCl, vehicle vs STZ). Endothelial function assessed via acetylcholine (ACh)-mediated relaxation was not affected by PTP1B deficiency but was reduced by STZ in Balb/C mice (63±5 vs 43±5% of precontraction, vehicle vs STZ). In PTP1B KO mice, STZ treatment did not affect maximum relaxation (56±7 vs 58±7% of preconstriction, vehicle vs STZ) but increased ACh sensitivity (logEC50 7.4±0.3 vs 8.2±0.2, vehicle vs STZ). Western blot analysis revealed a trend towards increased baseline Akt activation without changes in eNOS expression or activation. These data indicate that PTP1B deletion protects against the harmful vascular effects of type I diabetes." @default.
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- W198975449 date "2010-04-01" @default.
- W198975449 modified "2023-09-24" @default.
- W198975449 title "Deletion of protein tyrosine phosphatase 1B (PTP1B) prevents type 1 diabetes‐induced endothelial dysfunction." @default.
- W198975449 doi "https://doi.org/10.1096/fasebj.24.1_supplement.1037.7" @default.
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