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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)
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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
2016-04-01 16:40:39
date last changed
2022-01-28 21:23:05
@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}},
}