Editorials |
From the Department of Pharmacology and Toxicology, Michigan State University, East Lansing.
Correspondence to William F. Jackson, PhD, Dept. of Pharmacology and Toxicology, Michigan State University, B420 Life Sciences Bldg, East Lansing, MI 48824. E-mail jacks783@msu.edu
See related article, pages 12801287
Key Words: potassium channels vascular smooth muscle proliferation cell division KV.3.4 KCNC4
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Potassium channels play a major role in the immediate and long term regulation of vascular smooth muscle function.1 The activity of these ion channels determines and regulates cell membrane potential, which, in turn, regulates the open state probability of voltage-gated Ca2+ channels, Ca2+ influx, and intracellular Ca2+. The concentration of intracellular Ca2+ not only regulates the immediate contractile responses of smooth muscle cells (ie, vascular tone),1 but also the long term responses of these cells through control of gene expression.2 By their effect on membrane potential, K+ channels also establish the electrochemical gradient that determines the movement of other ions across the plasma membrane. In addition, potassium channels participate significantly in cell volume regulation.3
Over the past two decades it has become apparent that K+ channels also play an important role in cell proliferation.48 In vascular smooth muscle cells, investigators have identified increased expression of intermediate conductance, Ca2+-activated K+ (IKCa) channels (KCa3.1, locus: KCNN4) associated with proliferation,4 and recent studies have shown that selective inhibition of these channels prevents vascular smooth muscle proliferation associated with injury-induced restenosis.9 The study by Miguel-Velado et al in this issue of Circulation Research10 confirms an important role for K+ channels in vascular smooth muscle cell proliferation. The authors extend this area by showing that Kv3.4 channel (locus: KCNC4) expression is increased in proliferating smooth muscle cells from human uterine artery and that blockade of these channels inhibits proliferation. These KV channels also have been implicated in proliferation of an oral squamous
Related Article:
Circ. Res. 2005 97: 1280-1287.
This article has been cited by other articles:
![]() |
X. Bai, J. Ma, Z. Pan, Y.-H. Song, S. Freyberg, Y. Yan, D. Vykoukal, and E. Alt Electrophysiological properties of human adipose tissue-derived stem cells Am J Physiol Cell Physiol, November 1, 2007; 293(5): C1539 - C1550. [Abstract] [Full Text] [PDF] |
||||
|
Circulation Research Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 2005 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |