Mechanism of potentiation by tea epigallocatechin of contraction in porcine coronary artery: The role of protein kinase C delta-mediated CPI-17 phosphorylation

作者：Obara Kazuo^*; Ukai Kiyotaka; Ishikawa Tomohisa

来源：European Journal of Pharmacology, 2011, 668(3): 414-418.

DOI：10.1016/j.ejphar.2011.07.028

• Epigallocatechin
• Contractile potentiation
• CPI-17
• Protein kinase C delta
• Tea catechin
• Pig coronary artery

The effects of green tea catechins, (+)- and (-)-catechins (C), (-)-epicatechin (EC), (-)-epicatechin gallate (ECG), (-)-epigallocatechin (EGC), and (-)-epigallocatechin gallate (EGCG), on vascular contractility were investigated in porcine coronary artery. At the concentration of 200 mu M, only EGC, but not other catechins, potentiated high K(+)-induced contraction in a concentration-dependent manner, although EGC by itself did not produce contraction. The potentiator effect of EGC was still observed in endothelium-denuded preparations. Moreover, EGC increased the translocation of protein kinase C delta (PKC delta) from the cytosol to the plasma membrane and increased phosphorylations of 17-kDa PKC-potentiated protein phosphatase inhibitor protein (CPI-17) and myosin light chain (MLC(20)). These effects of EGC were inhibited by the PKC delta inhibitor rottlerin, but not by the conventional PKC inhibitor Go6976. These results suggest that EGC activates PKCS, leading to the phosphorylation of CPI-17, which in turn inhibits myosin light chain phosphatase and increases MLC(20) phosphorylation. The series of events would increase Ca(2+) sensitivity of contractile elements, thereby augmenting high K(+)-induced vascular contraction.

• 出版日期2011-10-15