Advanced

Long-term effects of intracellular calcium and growth factors on excitation and contraction in smooth muscle

Hellstrand, Per LU (1998) In Acta Physiologica Scandinavica 164(4). p.637-644
Abstract
Modulation of vascular smooth muscle cells from a contractile to a synthetic phenotype is thought to be important in the development of the atherosclerotic lesion. Such modulation depends on growth factors and is influenced by cell-cell and cell-matrix interactions. Whereas smooth muscle cells in the vessel wall are contractile, dispersed cells in culture rapidly modulate to synthetic phenotype, which complicates long-term in vitro studies. In contrast, vascular segments or smooth muscle strips in organ culture can maintain contractility for at least a week, sufficient for studies involving altered metabolism or protein expression. Examples are effects of endogenous polyamines on membrane ion channels and excitation-contraction coupling.... (More)
Modulation of vascular smooth muscle cells from a contractile to a synthetic phenotype is thought to be important in the development of the atherosclerotic lesion. Such modulation depends on growth factors and is influenced by cell-cell and cell-matrix interactions. Whereas smooth muscle cells in the vessel wall are contractile, dispersed cells in culture rapidly modulate to synthetic phenotype, which complicates long-term in vitro studies. In contrast, vascular segments or smooth muscle strips in organ culture can maintain contractility for at least a week, sufficient for studies involving altered metabolism or protein expression. Examples are effects of endogenous polyamines on membrane ion channels and excitation-contraction coupling. While smooth muscle tissue is well preserved in serum-free culture, growth stimulation with fetal calf serum (FCS) causes multiple effects, including decreased contractility, ultrastructural changes, decreased expression of L-type Ca2+ channels, and increased SR release of Ca2+ via ryanodine receptors. These are all consequences of increased basal [Ca2+]i caused by FCS, as they are reversed by culture with verapamil in a concentration (1 microM) that does not inhibit stimulation of DNA and protein synthesis by FCS. The effects of FCS on contractility and Ca2+ channel expression are mimicked in serum-free culture with increased [Ca2+]i. Contractile protein patterns, including myosin isoform composition, are unaffected by FCS, suggesting that reversal to synthetic phenotype is limited and not the immediate cause of decreased contractility. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
in
Acta Physiologica Scandinavica
volume
164
issue
4
pages
637 - 644
publisher
Wiley-Blackwell
external identifiers
  • pmid:9887985
  • scopus:0032430714
ISSN
0001-6772
language
English
LU publication?
yes
id
0bab5cb3-0ee1-4f89-9272-326e8f809bac (old id 1113378)
date added to LUP
2008-07-14 17:06:35
date last changed
2017-01-01 07:11:57
@article{0bab5cb3-0ee1-4f89-9272-326e8f809bac,
  abstract     = {Modulation of vascular smooth muscle cells from a contractile to a synthetic phenotype is thought to be important in the development of the atherosclerotic lesion. Such modulation depends on growth factors and is influenced by cell-cell and cell-matrix interactions. Whereas smooth muscle cells in the vessel wall are contractile, dispersed cells in culture rapidly modulate to synthetic phenotype, which complicates long-term in vitro studies. In contrast, vascular segments or smooth muscle strips in organ culture can maintain contractility for at least a week, sufficient for studies involving altered metabolism or protein expression. Examples are effects of endogenous polyamines on membrane ion channels and excitation-contraction coupling. While smooth muscle tissue is well preserved in serum-free culture, growth stimulation with fetal calf serum (FCS) causes multiple effects, including decreased contractility, ultrastructural changes, decreased expression of L-type Ca2+ channels, and increased SR release of Ca2+ via ryanodine receptors. These are all consequences of increased basal [Ca2+]i caused by FCS, as they are reversed by culture with verapamil in a concentration (1 microM) that does not inhibit stimulation of DNA and protein synthesis by FCS. The effects of FCS on contractility and Ca2+ channel expression are mimicked in serum-free culture with increased [Ca2+]i. Contractile protein patterns, including myosin isoform composition, are unaffected by FCS, suggesting that reversal to synthetic phenotype is limited and not the immediate cause of decreased contractility.},
  author       = {Hellstrand, Per},
  issn         = {0001-6772},
  language     = {eng},
  number       = {4},
  pages        = {637--644},
  publisher    = {Wiley-Blackwell},
  series       = {Acta Physiologica Scandinavica},
  title        = {Long-term effects of intracellular calcium and growth factors on excitation and contraction in smooth muscle},
  volume       = {164},
  year         = {1998},
}