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Titolo:
Signal transduction in smooth muscle - Selected contribution: Insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle
Autore:
Sandu, OA; Ito, M; Begum, N;
Indirizzi:
Winthrop Univ Hosp, Diabet Res Lab, Mineola, NY 11501 USA Winthrop Univ Hosp Mineola NY USA 11501 et Res Lab, Mineola, NY 11501 USA SUNY Stony Brook, Sch Med, Stony Brook, NY 11794 USA SUNY Stony Brook Stony Brook NY USA 11794 Med, Stony Brook, NY 11794 USA Mie Univ, Sch Med, Dept Internal Med 1, Tsu, Mie, Japan Mie Univ Tsu Mie Japan iv, Sch Med, Dept Internal Med 1, Tsu, Mie, Japan
Titolo Testata:
JOURNAL OF APPLIED PHYSIOLOGY
fascicolo: 3, volume: 91, anno: 2001,
pagine: 1475 - 1482
SICI:
8750-7587(200109)91:3<1475:STISM->2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
LIGHT-CHAIN PHOSPHATASE; PROTEIN-KINASE; CA2+ SENSITIZATION; NITRIC-OXIDE; SUBUNIT COMPOSITION; CELLS; PHOSPHORYLATION; TRANSLOCATION; HYPERTENSION; CONTRACTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Begum, N Winthrop Univ Hosp, Diabet Res Lab, 222 Stn Plaza N,Suite 511-B, Mineola, NY 11501 USA Winthrop Univ Hosp 222 Stn Plaza N,Suite 511-B Mineola NY USA 11501
Citazione:
O.A. Sandu et al., "Signal transduction in smooth muscle - Selected contribution: Insulin utilizes NO/cGMP pathway to activate myosin phosphatase via Rho inhibition in vascular smooth muscle", J APP PHYSL, 91(3), 2001, pp. 1475-1482

Abstract

Our laboratory has recently demonstrated that insulin induces relaxation of vascular smooth muscle cells (VSMCs) by activating myosin-bound phosphatase (MBP) and by inhibiting Rho kinase (Begum N, Duddy N, Sandu OA, Reinzie J, and Ragolia L. Mol Endocrinol 14: 1365-1376, 2000). In this study, we tested the hypothesis that insulin via the nitric oxide (NO)/cGMP pathway mayinactivate Rho, resulting in a decrease in phosphorylation of the myosin-bound subunit (MBSThr695) of MBP and in its activation. Treatment of confluent serum-starved VSMCs with insulin prevented thrombin-induced increases inmembrane-associated RhoA, Rho kinase activation, and site-specific phosphorylation of MBSThr695 of MBP and caused MBP activation. Preexposure to N-G-monomethyl-L-arginine, a NO synthase inhibitor, and R-p-8-(4-chlorophenylthio) cGMP, a cGMP antagonist, attenuated insulin's inhibitory effect on Rho translocation and restored thrombin-mediated Rho kinase activation and site-specific MBSThr695 phosphorylation, resulting in MBP inactivation. In contrast, 8-bromo-cGMP, a cGMP agonist, mimicked insulin's inhibitory effects by abolishing thrombin-mediated Rho signaling and promoted dephosphorylationof MBSThr695. Furthermore, expression of a dominant-negative RhoA decreased basal as well as thrombin-induced MBSThr695 phosphorylation and caused insulin activation of MBP. Collectively, these results indicate that insulin inhibits Rho signaling by decreasing RhoA translocation via the NO/cGMP signaling pathway to cause MBP activation via site-specific dephosphorylation of its regulatory subunit MBS.

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Documento generato il 04/04/20 alle ore 11:07:04