Rho and smooth muscle cell phenotype

Worth, N. F., Rolfe, B. E. and Campbell, G. R. (2003). Rho and smooth muscle cell phenotype. In: Atherosclerosis Supplements. 13th International Atherosclerosis Symposium, Kyoto, Japan, (180-180). 28 September - 2 October 2004. doi:10.1016/S1567-5688(03)90774-4


Author Worth, N. F.
Rolfe, B. E.
Campbell, G. R.
Title of paper Rho and smooth muscle cell phenotype
Conference name 13th International Atherosclerosis Symposium
Conference location Kyoto, Japan
Conference dates 28 September - 2 October 2004
Proceedings title Atherosclerosis Supplements   Check publisher's open access policy
Place of Publication Amsterdam, The Netherlands
Publisher Elsevier
Publication Year 2003
DOI 10.1016/S1567-5688(03)90774-4
ISSN 1567-5688
Volume 4
Issue 2
Start page 180
End page 180
Total pages 1
Language eng
Abstract/Summary Smooth muscle cell (SMC) phenotypic modulation from the mature ’contractile’ to a less differentiated ’synthetic’ phenotype involves not only altered expression but also a reorganisation of contractile and cytoskeletal proteins. Objective: To investigate the role of RhoA, a known regulator of the actin cytoskeleton, in SMC phenotypic regulation. Methods: Rho transcription (RT-PCR), expression (Western analysis) and activation (membrane translocation or Rho ’pull-down’ assay) was investigated in cultured rabbit aortic SMC during phenotypic modulation, and under the influence of known SM-regulatory proteins (thrombin, heparin and TGF- β). Rho’s effect on cell morphology was examined by transient transfection of ’synthetic’ state SMC with either constitutively active Rho (Val14RhoA) or its inhibitor, C3 transferase. Results: RhoA transcription was elevated in the first 3 days of primary culture, and protein expression peaked at 2 days post-confluence when SMC return to a more ’contractile’ state. However, RhoA showed augmented activation at three time-points in primary culture: the transition point when SMCs enter logarithmic growth and are highly motile, upon reaching quiescence, and when they return to a more ’contractile’ state. Thrombin, heparin and TGF-β activated RhoA in ’synthetic’ state SMCs. Transfection with Val14RhoA caused a dramatic decrease in SMC size and a reorganization of cytoskeletal proteins, reminiscent of the ’contractile’ phenotype. Specific inhibition of endogenous Rho by C3 transferase resulted in an almost complete loss of contractile proteins. Conclusion: These data indicate that Rho is an important determining factor of SMC functional state.
Subjects E4
321003 Cardiology (incl. Cardiovascular Diseases)
730106 Cardiovascular system and diseases
Q-Index Code E4
Additional Notes 3SY07-6

 
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Created: Mon, 27 Aug 2007, 13:01:25 EST