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Mechanisms related to NO-induced motility in differentiated rat aortic smooth muscle cells. | LitMetric

AI Article Synopsis

  • Nitric oxide (NO) inhibits vascular cell growth and movement, but its role varies under different conditions, such as high fat diet and hyperinsulinemia.
  • NO and insulin together increase the secretion of angiotensin II (ANG II), enhancing cell movement (motogenesis) and reducing levels of protein tyrosine phosphatase (PTP)1B.
  • The study highlights that the cooperative effects of NO and insulin on motogenesis depend on ANG II signaling, PTP1B suppression, and increased activity of phosphatidyl inositol 3-kinase (PI3K)-δ and Src homology-2 domain PTP (SHP2).

Article Abstract

Nitric oxide (NO) is thought to play an important role as an inhibitor of vascular cell proliferation, motility, and neointima formation. This effect is mediated, in part, via the upregulation of protein tyrosine phosphatase (PTP)1B. Conversely, studies have reported that in presumably hyperinsulinemic mice fed a high-fat diet, NO enhances vascular remodeling, whereas a deficit of NO attenuates vascular remodeling. We have reported that in differentiated cultured smooth muscle cells treated with insulin, NO induces a motogenic effect that is dependent on Src homology-2 domain PTP 2 (SHP2) upregulation. In the present study, we describe novel mechanisms relevant to the motogenic effect of NO. Treatment of cultured cells with the selective angiontensin type 1 receptor antagonist losartan, but not with the selective angiotensin type 2 receptor antagonist PD-123319, blocked the comotogenic capacity of NO and insulin. Insulin and NO increased the secretion of ANG II into the culture media by 2- and 2.5-fold (P < 0.05), respectively, whereas treatment of cells with ANG II uncovered the motogenic effect of NO (1.4-fold above control, P < 0.05) and decreased the levels of PTP1B to 45% of control (P < 0.05). Suppression of PTP1B function was sufficient to uncover the motogenic effect of NO. The capacity of insulin to suppress PTP1B activity was blocked by losartan, implicating ANG II function in mediating this effect. Both insulin and ANG II induced the upregulation of phosphatidyl inositol 3-kinase (PI3K)-δ by two- to threefold (P < 0.05), and this effect was both necessary and sufficient to uncover NO-induced motogenesis. Finally, suppression of PTP1B function potentiated, whereas overexpression of PTP1B inhibited, SHP2-induced motogenesis. These results support the hypothesis that the comotogenic effect of insulin and NO occurs via an ANG II-mediated effect involving the suppression of PTP1B and upregulation of PI3K-δ and SHP2.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3023252PMC
http://dx.doi.org/10.1152/ajpheart.00342.2010DOI Listing

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