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Lysophosphatidylcholine Increases Ca Current via Activation of Protein Kinase C in Rabbit Portal Vein Smooth Muscle Cells.

Authors
 Seungsoo Jung  ;  Youngho Lee  ;  Sungsik Han  ;  Youngwhan Kim  ;  Taiksang Nam  ;  Ducksun Ahn 
Citation
 Korean Journal of Physiology & Pharmacology, Vol.12(1) : 31-35, 2008 
Journal Title
 Korean Journal of Physiology & Pharmacology 
ISSN
 1226-4512 
Issue Date
2008
Keywords
Ca2+ current ; Lysophosphatidylcholine ; Protein kinase C ; Vascular smooth muscle
Abstract
Lysophosphatidylcholine (LPC), a metabolite of membrane phospholipids by phospholipase A(2), has been considered responsible for the development of abnormal vascular reactivity during atherosclerosis. Ca(2+) influx was shown to be augmented in atherosclerotic artery which might be responsible for abnormal vascular reactivity. However, the mechanism underlying Ca(2+) influx change in atherosclerotic artery remains undetermined. The purpose of the present study was to examine the effects of LPC on L-type Ca(2+) current (I(Ca(L))) activity and to elucidate the mechanism of LPC-induced change of I(Ca(L)) in rabbit portal vein smooth muscle cells using whole cell patch clamp. Extracellular application of LPC increased I(Ca(L)) through whole test potentials, and this effect was readily reversed by washout. Steady state voltage dependency of activation or inactivation properties of I(Ca(L)) was not significantly changed by LPC. Staurosporine (100 nM) or chelerythrine (3 microM), which is a potent inhibitor of PKC, significantly decreased basal I(Ca(L)), and LPC-induced increase of I(Ca(L)) was significantly suppressed in the presence of PKC inhibitors. On the other hand, application of PMA, an activator of PKC, increased basal I(Ca(L)) significantly, and LPC-induced enhancement of I(Ca(L)) was abolished by pretreatment of the cells with PMA. These findings suggest that LPC increased I(Ca(L)) in vascular smooth muscle cells by a pathway that involves PKC, and that LPC-induced increase of I(Ca(L)) might be, at least in part, responsible for increased Ca(2+) influx in atherosclerotic artery
Files in This Item:
T200800503.pdf Download
DOI
10.4196/kjpp.2008.12.1.31
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Physiology (생리학교실) > 1. Journal Papers
Yonsei Authors
Kim, Young Hwan(김영환)
Nam, Taick Sang(남택상)
Ahn, Duk Sun(안덕선) ORCID logo https://orcid.org/0000-0001-9351-6951
Lee, Young Ho(이영호) ORCID logo https://orcid.org/0000-0002-5749-1045
Chung, Seung Soo(정승수) ORCID logo https://orcid.org/0000-0002-3119-9628
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/106684
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