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Stretch-dependent growth and differentiation in vascular smooth muscle: role of the actin cytoskeleton

Hellstrand, Per LU and Albinsson, Sebastian LU (2005) In Canadian Journal of Physiology and Pharmacology 83(10). p.869-875
Abstract
The smooth muscle cells in the vascular wall are constantly exposed to distending forces from the intraluminal pressure. A rise in blood pressure triggers growth of the vessel wall, which is characterized primarily by hypertrophy of smooth muscle cells with maintained differentiation in a contractile phenotype. Growth factor stimulation of dissociated smooth muscle cells, on the other hand, causes proliferative growth with loss of contractility. This type of response is also found in neointima development following angioplasty and in atherosclerotic lesions. An intact tissue environment is therefore critical for preserved differentiation. Recent advances point to a role of actin polymerization in the expression of smooth muscle... (More)
The smooth muscle cells in the vascular wall are constantly exposed to distending forces from the intraluminal pressure. A rise in blood pressure triggers growth of the vessel wall, which is characterized primarily by hypertrophy of smooth muscle cells with maintained differentiation in a contractile phenotype. Growth factor stimulation of dissociated smooth muscle cells, on the other hand, causes proliferative growth with loss of contractility. This type of response is also found in neointima development following angioplasty and in atherosclerotic lesions. An intact tissue environment is therefore critical for preserved differentiation. Recent advances point to a role of actin polymerization in the expression of smooth muscle differentiation marker genes, in concert with serum response factor (SRF) and cofactors, such as myocardin. Stretch of intact venous smooth muscle activates Rho and inhibits the actin filament severing factor cofilin, resulting in increased actin polymerization. Concomitantly, the rates of synthesis of SRF-regulated differentiation markers, such as SM22 alpha, calponin, and alpha-actin, are increased. This increase in differentiation signals is parallel with activation of the mitogen-activated protein (MAP) kinase pathway. Thus stretch-induced growth in a maintained contractile phenotype occurs by dual activation of signal pathways regulating both growth and differentiation. A current challenge is to identify sites of crosstalk between these pathways in intact smooth muscle tissue. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
ERK, stretch, hypertension, caveolae, Rho
in
Canadian Journal of Physiology and Pharmacology
volume
83
issue
10
pages
869 - 875
publisher
National Research Council Canada
external identifiers
  • wos:000234416100010
  • pmid:16333359
  • scopus:32544456762
ISSN
0008-4212
DOI
10.1139/y05-061
language
English
LU publication?
yes
id
8239fa89-d876-4d08-9828-a49909cb914c (old id 210314)
date added to LUP
2007-08-24 14:06:15
date last changed
2017-08-27 03:55:21
@article{8239fa89-d876-4d08-9828-a49909cb914c,
  abstract     = {The smooth muscle cells in the vascular wall are constantly exposed to distending forces from the intraluminal pressure. A rise in blood pressure triggers growth of the vessel wall, which is characterized primarily by hypertrophy of smooth muscle cells with maintained differentiation in a contractile phenotype. Growth factor stimulation of dissociated smooth muscle cells, on the other hand, causes proliferative growth with loss of contractility. This type of response is also found in neointima development following angioplasty and in atherosclerotic lesions. An intact tissue environment is therefore critical for preserved differentiation. Recent advances point to a role of actin polymerization in the expression of smooth muscle differentiation marker genes, in concert with serum response factor (SRF) and cofactors, such as myocardin. Stretch of intact venous smooth muscle activates Rho and inhibits the actin filament severing factor cofilin, resulting in increased actin polymerization. Concomitantly, the rates of synthesis of SRF-regulated differentiation markers, such as SM22 alpha, calponin, and alpha-actin, are increased. This increase in differentiation signals is parallel with activation of the mitogen-activated protein (MAP) kinase pathway. Thus stretch-induced growth in a maintained contractile phenotype occurs by dual activation of signal pathways regulating both growth and differentiation. A current challenge is to identify sites of crosstalk between these pathways in intact smooth muscle tissue.},
  author       = {Hellstrand, Per and Albinsson, Sebastian},
  issn         = {0008-4212},
  keyword      = {ERK,stretch,hypertension,caveolae,Rho},
  language     = {eng},
  number       = {10},
  pages        = {869--875},
  publisher    = {National Research Council Canada},
  series       = {Canadian Journal of Physiology and Pharmacology},
  title        = {Stretch-dependent growth and differentiation in vascular smooth muscle: role of the actin cytoskeleton},
  url          = {http://dx.doi.org/10.1139/y05-061},
  volume       = {83},
  year         = {2005},
}