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Differential dependence of stretch and shear stress signaling on caveolin-1 in the vascular wall

Albinsson, Sebastian LU ; Nordström, Ina LU ; Swärd, Karl LU and Hellstrand, Per LU (2008) In American Journal of Physiology: Cell Physiology 294. p.271-279
Abstract
The role of caveolae in stretch- vs. flow-induced vascular responses was investigated using caveolin-1 deficient (KO) mice. Portal veins were stretched longitudinally for 5 min (acute) or 72 h (organ culture). Basal ERK1/2 and Akt phosphorylation were increased in organ-cultured KO veins, as were protein synthesis and vessel wall cross-section. Stretch stimulated acute phosphorylation of ERK1/2 and long-term phosphorylation of focal adhesion kinase (FAK) and cofilin, but did not affect Akt phosphorylation. Protein synthesis, and particularly synthesis of smooth muscle differentiation markers, was increased by stretch. These effects did not differ in portal veins from KO and control mice, which also showed the same contractile response to... (More)
The role of caveolae in stretch- vs. flow-induced vascular responses was investigated using caveolin-1 deficient (KO) mice. Portal veins were stretched longitudinally for 5 min (acute) or 72 h (organ culture). Basal ERK1/2 and Akt phosphorylation were increased in organ-cultured KO veins, as were protein synthesis and vessel wall cross-section. Stretch stimulated acute phosphorylation of ERK1/2 and long-term phosphorylation of focal adhesion kinase (FAK) and cofilin, but did not affect Akt phosphorylation. Protein synthesis, and particularly synthesis of smooth muscle differentiation markers, was increased by stretch. These effects did not differ in portal veins from KO and control mice, which also showed the same contractile response to membrane depolarization and inhibition by the Rho kinase inhibitor Y-27632. KO carotid arteries had increased wall cross-section and responded to pressurization (120 mmHg) for 1 h with increased ERK1/2 but not Akt phosphorylation, similar to control arteries. Shear stress by flow for 15 min, on the other hand, increased phosphorylation of Akt in carotids from control but not KO mice. In conclusion, caveolin-1 contributes to a low basal ERK1/2 and Akt activity and is required for Akt-dependent signals in response to shear stress (flow), but is not essential for trophic effects of stretch (pressure) in the vascular wall. Key words: Hypertrophy, vasoconstriction, vascular smooth muscle, endothelium, nitric oxide. (Less)
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author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
vascular smooth muscle, endothelium, hypertrophy, vasoconstriction, nitric oxide
in
American Journal of Physiology: Cell Physiology
volume
294
pages
271 - 279
publisher
American Physiological Society
external identifiers
  • pmid:17989209
  • wos:000252507600031
  • scopus:38349182440
ISSN
1522-1563
DOI
10.1152/ajpcell.00297.2007
language
English
LU publication?
yes
id
8db18cfb-7ad5-455a-b1e4-f6d7981174dc (old id 1137826)
date added to LUP
2008-04-29 11:23:07
date last changed
2017-01-29 03:47:12
@article{8db18cfb-7ad5-455a-b1e4-f6d7981174dc,
  abstract     = {The role of caveolae in stretch- vs. flow-induced vascular responses was investigated using caveolin-1 deficient (KO) mice. Portal veins were stretched longitudinally for 5 min (acute) or 72 h (organ culture). Basal ERK1/2 and Akt phosphorylation were increased in organ-cultured KO veins, as were protein synthesis and vessel wall cross-section. Stretch stimulated acute phosphorylation of ERK1/2 and long-term phosphorylation of focal adhesion kinase (FAK) and cofilin, but did not affect Akt phosphorylation. Protein synthesis, and particularly synthesis of smooth muscle differentiation markers, was increased by stretch. These effects did not differ in portal veins from KO and control mice, which also showed the same contractile response to membrane depolarization and inhibition by the Rho kinase inhibitor Y-27632. KO carotid arteries had increased wall cross-section and responded to pressurization (120 mmHg) for 1 h with increased ERK1/2 but not Akt phosphorylation, similar to control arteries. Shear stress by flow for 15 min, on the other hand, increased phosphorylation of Akt in carotids from control but not KO mice. In conclusion, caveolin-1 contributes to a low basal ERK1/2 and Akt activity and is required for Akt-dependent signals in response to shear stress (flow), but is not essential for trophic effects of stretch (pressure) in the vascular wall. Key words: Hypertrophy, vasoconstriction, vascular smooth muscle, endothelium, nitric oxide.},
  author       = {Albinsson, Sebastian and Nordström, Ina and Swärd, Karl and Hellstrand, Per},
  issn         = {1522-1563},
  keyword      = {vascular smooth muscle,endothelium,hypertrophy,vasoconstriction,nitric oxide},
  language     = {eng},
  pages        = {271--279},
  publisher    = {American Physiological Society},
  series       = {American Journal of Physiology: Cell Physiology},
  title        = {Differential dependence of stretch and shear stress signaling on caveolin-1 in the vascular wall},
  url          = {http://dx.doi.org/10.1152/ajpcell.00297.2007},
  volume       = {294},
  year         = {2008},
}