A role for Rho in smooth muscle phenotypic regulation

Worth, N. F., Campbell, G. R. and Rolfe, B. E. (2001). A role for Rho in smooth muscle phenotypic regulation. In: Fuiko Numano and Michael Gimbrone, Annals of the New York Academy of Sciences: Proceedings of the 6th Saratoga International Conference on Atherosclerosis. 6th Saratoga International Conference on Atherosclerosis, Tokyo, Japan, (316-322). 3-6 April, 2001.


Author Worth, N. F.
Campbell, G. R.
Rolfe, B. E.
Title of paper A role for Rho in smooth muscle phenotypic regulation
Conference name 6th Saratoga International Conference on Atherosclerosis
Conference location Tokyo, Japan
Conference dates 3-6 April, 2001
Proceedings title Annals of the New York Academy of Sciences: Proceedings of the 6th Saratoga International Conference on Atherosclerosis   Check publisher's open access policy
Journal name Atherosclerosis VI   Check publisher's open access policy
Place of Publication New York
Publisher The Academy
Publication Year 2001
Sub-type Fully published paper
ISBN 1-57331-364-5
ISSN 0077-8923
Editor Fuiko Numano
Michael Gimbrone
Volume 947
Start page 316
End page 322
Total pages 7
Language eng
Abstract/Summary The role of the small GTP-binding protein Rho in the process of smooth muscle cell (SMC) phenotypic modulation was investigated using cultured rabbit aortic SMCs. Both Rho transcription and Rho protein expression were high for the first 3 days of culture ("contractile" state cells), with expression decreasing after change to the "synthetic" state and peaking upon return to the contractile phenotype. Activation of Rho (indicated by translocation to the membrane) also peaked upon return to the contractile state and was low in synthetic state SMCs. Transient transfection of synthetic state rabbit SMCs with constitutively active Rho (vall4rho) caused a dramatic decrease in cell size and reorganization of cytoskeletal proteins to resemble those of the contractile phenotype; alpha-actin and myosin adopted a tightly packed, highly organized arrangement, whereas vimentin localized to the immediate perinuclear region and focal adhesions were enlarged. Conversely, specific inhibition of endogenous Rho, by expression of C3 transferase, resulted in the complete loss of actin and myosin filaments without affecting the distribution of vimentin. Focal adhesions were reduced in number. Thus, Rho plays a key role in regulating SMC phenotypic expression.
Subjects C1
321003 Cardiology (incl. Cardiovascular Diseases)
730106 Cardiovascular system and diseases
Keyword Rho
smooth mucsle cells
modulation
contractile state
synthetic state
C3 transferase
Q-Index Code C1
Additional Notes Source: ATHEROSCLEROSIS VI Book Series: ANNALS OF THE NEW YORK ACADEMY OF SCIENCES Volume: 947 Pages: 316-322 Published: 2001

Document type: Conference Paper
Collection: School of Biomedical Sciences Publications
 
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