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Second Congress of Cardiology and Angiology of Bosnia & Herzegovina

 

PI-3 KINASE/AKT/PKB SIGNAL TRANSDUCTION PATHWAY MEDIATES NOREPINEPHRINE-INDUCED VASCULAR SMOOTH MUSCLE CELL PROLIFERATION
F. Ljuca1, Dž. Ljuca2 and S. Nuhbegović1
Department of Physiology, School of Medicine, Department of Gynecology and Obstetrics, Clinical Center University of Tuzla, Bosnia and Herzegovina

Introduction: Norepinephrine (NE) by binding primarily a1 adrenergic receptors promotes vascular smooth muscle cell (VSMC) proliferation. Activated PI-3 kinase/AKT/PKB signal transduction pathway has been implicated in cell growth and VSMC proliferation. Aim: To determine whether NE activates PI-3 kinase/AKT/PKB signal transduction pathway in rabbit VSMC and by which mechanism.

Methods: PI-3 kinase activity has been measured by PI-3 kinase assay; MAPK, AKT/PKB activities by Western blotting analysis using antiphospho-MAPK and antiphospho-AKT/PKB antibodies and VSMC proliferation by 3H-thymidine incorporation. All assays have been determined in VSMC treated by NE in presence or absance of different Ras, MEK, MAPK and PI-3 kinase inhibitors. Results: NE treatment significantly induced VSMC proliferation. PI-3 kinase, AKT/PKB and Ras/MEK/MAPK activities have been highly elevated in NE treated cells. However, when cells have been treated by NE in presence of FPT III, a Ras inhibitor, PI-3 kinase andAKT/PKB activities were decreased.

Conclusion: NE induces VSMC proliferation by activation Ras/MEK/MAPK signal transduction pathway that mediates PI-3 kinase/AKT/PKB activation.

Drugi kongres kardiologa i angiologa Bosne i Hercegovine
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