کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2567889 | 1561094 | 2007 | 6 صفحه PDF | دانلود رایگان |
It has been reported that CPI-17 (protein kinase C (PKC)-potentiated inhibitory protein for heterotrimeric myosin light chain phosphatase (MLCP) of 17 kDa) was phosphorylated by excitatory agonists in smooth muscle contraction. However, endothelin-1 (ET-1)-mediated regulation of CPI-17 in bronchial smooth muscle has not been documented. We therefore investigated whether phosphorylation of CPI-17 is induced by ET-1 in rat bronchial smooth muscle. Moreover, the role of Rho kinase (ROCK; Rho-associated coiled-coil forming protein kinase) is investigated in phosphorylation of CPI-17 induced by ET-1 in rat bronchial smooth muscle. The ET-1-induced contraction was attenuated by Y-27632 (10−6 M), a ROCK inhibitor. ET-1 induced a phosphorylation of CPI-17 with a phosphorylation of myosin light chain (MLC); those phosphorylation responses were significantly inhibited by Y-27632 (10−6 M). These findings suggest that the activation of ROCK is involved in force development and CPI-17 phosphorylation induced by ET-1 stimulation in rat bronchial smooth muscle. Thus, RhoA/ROCK/CPI-17 pathway is considered to play an important role in the ET-1-induced Ca2+ sensitisation of bronchial smooth muscle contraction.
Journal: Pulmonary Pharmacology & Therapeutics - Volume 20, Issue 6, December 2007, Pages 734–739