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Roles of Protein Tyrosine Phosphatase 1B (PTP1B) in Vascular Function and Remodeling In Vivo

Previous studies have indicated that PTP1B is a crucial negative regulator of insulin signaling. Importantly, PTP1B is also implicated in vascular smooth muscle cell (VSMC) growth and proliferation. Our recent findings suggest that PTP1B impairs insulin‐induced activation of anti‐mitogenic pathways (Akt) while enhancing insulin‐induced activation of mitogenic pathways (p42/44 MAPK) in rat aortic VSMC. However, little is known about the role of PTP1B modulation of vascular function including the insulin signaling pathways in the vasculature in vivo. Here, we test the hypothesis that deletion of PTP1B improves vascular function and prevents vascular remodeling in vivo. The relaxant response to acetylcholine was marked improved in aortic rings from PTP1B knockout (KO) mice compared to aortas from wild type (WT) mice. This improvement in endothelial function did not significantly influence vascular remodeling in the common carotid artery which was not different between WT and PTP1B KO mice. Finally, we observed that the basal activations of Akt and p44/p42 MAPK in aorta were not statistically different between PTP1B KO and WT mice. We conclude that loss of PTP1B function improves vascular function but under basal conditions has no effect in vascular remodeling. Further roles for PTP1B may be more clearly manifested in disease states such as diabetes and obesity. NIH Grants HL58139 (MBM), AHA SDG (ABB)