Stretch-induced contractile differentiation of vascular smooth muscle: sensitivity to actin polymerization inhibitors.
(2003) In American Journal of Physiology: Cell Physiology 284(6). p.1387-1396- Abstract
- Signaling mechanisms for stretch-dependent growth and differentiation of vascular smooth muscle were investigated in mechanically loaded rat portal veins in organ culture. Stretch-dependent protein synthesis was found to depend on endogenous release of angiotensin II. Autoradiography after [35S]methionine incorporation revealed stretch-dependent synthesis of several proteins, of which SM22 and actin were particularly prominent. Inhibition of RhoA activity by cell-permeant C3 toxin increased tissue mechanical compliance and reduced stretch-dependent extracellular signal-regulated kinase (ERK)1/2 activation, growth, and synthesis of actin and SM22, suggesting a role of the actin cytoskeleton. In contrast, inhibition of Rho-associated kinase... (More)
- Signaling mechanisms for stretch-dependent growth and differentiation of vascular smooth muscle were investigated in mechanically loaded rat portal veins in organ culture. Stretch-dependent protein synthesis was found to depend on endogenous release of angiotensin II. Autoradiography after [35S]methionine incorporation revealed stretch-dependent synthesis of several proteins, of which SM22 and actin were particularly prominent. Inhibition of RhoA activity by cell-permeant C3 toxin increased tissue mechanical compliance and reduced stretch-dependent extracellular signal-regulated kinase (ERK)1/2 activation, growth, and synthesis of actin and SM22, suggesting a role of the actin cytoskeleton. In contrast, inhibition of Rho-associated kinase by Y-27632 did not reduce ERK1/2 phosphorylation or actin and SM22 synthesis and did not affect tissue mechanical compliance but still inhibited overall growth. The actin polymerization inhibitors latrunculin B and cytochalasin D both inhibited growth and caused increased tissue compliance. Whereas latrunculin B concentration-dependently reduced actin and SM22 synthesis, cytochalasin D did so at low (10-8 M) but not at high (10-6 M) concentration. The results show that stretch stabilizes the contractile smooth muscle phenotype. Stretch-dependent differentiation marker expression requires an intact cytoskeleton for stretch sensing, control of protein expression via the level of unpolymerized G-actin, or both. (Less)
Please use this url to cite or link to this publication:
https://lup.lub.lu.se/record/114174
- author
- Zeidan, Asad LU ; Nordström, Ina LU ; Albinsson, Sebastian LU ; Malmqvist, Ulf ; Swärd, Karl LU and Hellstrand, Per LU
- organization
- publishing date
- 2003
- type
- Contribution to journal
- publication status
- published
- subject
- in
- American Journal of Physiology: Cell Physiology
- volume
- 284
- issue
- 6
- pages
- 1387 - 1396
- publisher
- American Physiological Society
- external identifiers
-
- wos:000182678000007
- pmid:12734104
- scopus:0038612851
- ISSN
- 1522-1563
- DOI
- 10.1152/ajpcell.00508.2002
- language
- English
- LU publication?
- yes
- id
- 5c5ce5a0-6607-43ae-8621-572c8ac2a2a6 (old id 114174)
- alternative location
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12734104&dopt=Abstract
- date added to LUP
- 2016-04-01 17:12:26
- date last changed
- 2025-04-04 14:33:46
@article{5c5ce5a0-6607-43ae-8621-572c8ac2a2a6,
abstract = {{Signaling mechanisms for stretch-dependent growth and differentiation of vascular smooth muscle were investigated in mechanically loaded rat portal veins in organ culture. Stretch-dependent protein synthesis was found to depend on endogenous release of angiotensin II. Autoradiography after [35S]methionine incorporation revealed stretch-dependent synthesis of several proteins, of which SM22 and actin were particularly prominent. Inhibition of RhoA activity by cell-permeant C3 toxin increased tissue mechanical compliance and reduced stretch-dependent extracellular signal-regulated kinase (ERK)1/2 activation, growth, and synthesis of actin and SM22, suggesting a role of the actin cytoskeleton. In contrast, inhibition of Rho-associated kinase by Y-27632 did not reduce ERK1/2 phosphorylation or actin and SM22 synthesis and did not affect tissue mechanical compliance but still inhibited overall growth. The actin polymerization inhibitors latrunculin B and cytochalasin D both inhibited growth and caused increased tissue compliance. Whereas latrunculin B concentration-dependently reduced actin and SM22 synthesis, cytochalasin D did so at low (10-8 M) but not at high (10-6 M) concentration. The results show that stretch stabilizes the contractile smooth muscle phenotype. Stretch-dependent differentiation marker expression requires an intact cytoskeleton for stretch sensing, control of protein expression via the level of unpolymerized G-actin, or both.}},
author = {{Zeidan, Asad and Nordström, Ina and Albinsson, Sebastian and Malmqvist, Ulf and Swärd, Karl and Hellstrand, Per}},
issn = {{1522-1563}},
language = {{eng}},
number = {{6}},
pages = {{1387--1396}},
publisher = {{American Physiological Society}},
series = {{American Journal of Physiology: Cell Physiology}},
title = {{Stretch-induced contractile differentiation of vascular smooth muscle: sensitivity to actin polymerization inhibitors.}},
url = {{http://dx.doi.org/10.1152/ajpcell.00508.2002}},
doi = {{10.1152/ajpcell.00508.2002}},
volume = {{284}},
year = {{2003}},
}