Endothelin-1 induced vascular smooth muscle cell proliferation is mediated by cytochrome p-450 arachidonic acid metabolites.
作者： Farid Ljuca , Gorazd Drevenšek
关键词: Baicalein 、 Molecular biology 、 Cyclooxygenase 、 Medicine 、 Endothelins 、 Biochemistry 、 Receptor 、 Endothelin 1 、 Vascular smooth muscle 、 Arachidonic acid 、 Cell growth
摘要: Endothelins (ETs) are a family of three peptides (ET-1, ET-2, ET-3) that implicated in the physiological control vascular smooth muscle cell (VSMC) and myocardial contractility growth. ET-1 is vasoactive peptide acts via ET-A receptors coupling inducing contraction. involved development maintenance hypertension. Aim this study was to investigate whether can induce proliferation through arachidonic acid (AA) metabolites formed cytochrome P-450 (CYP-450). VSMC measured by [ 3 H]thymidine incorporation cultured cells treated (10 l00 nmol/L) presence different inhibitors CYP-450 (17-ODYA 5 μmol/L), lipoxygenase (LO) (baicalein 20 μmol/L) cyclooxygenase (COX) (indomethacin μmol/L). 100 induced effect attenuated inhibitor (17-ODYA) (baicalein) but not (indomethacin). LO AA, 20-hydroxyeicosatetraenoic (HETE) 12-HETE increased VSMC. Inhibitors MAP kinase (PD-98059 50 cPLA2 (MAFP as well 20-HETE proliferation. These results suggest AA mediates
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