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Vol. 40, No. 4, 2003
Issue release date: July–August 2003
Section title: Research Paper
J Vasc Res 2003;40:378–388
(DOI:10.1159/000072702)

Signal Transduction in Matrix Contraction and the Migration of Vascular Smooth Muscle Cells in Three-Dimensional Matrix

Li S. · Moon J.J. · Miao H. · Jin G. · Chen B.P.C. · Yuan S. · Hu Y. · Usami S. · Chien S.
aDepartment of Bioengineering, University of California, Berkeley, Calif., and bDepartment of Bioengineering and Whitaker Institute of Biomedical Engineering, University of California, San Diego, La Jolla, Calif., USA

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Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: 1/24/2003
Accepted: 4/23/2003
Published online: 9/26/2003

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR

Abstract

The interaction of vascular smooth muscle cells (SMCs) and extracellular matrix plays important roles in vascular remodeling. We investigated the signaling pathways involved in SMC-induced matrix contraction and SMC migration in three-dimensional (3D) collagen matrix. Matrix contraction is inhibited by the disruption of actin filaments but not microtubules. Therefore, we investigated the roles of signaling pathways related to actin filaments in matrix contraction. SMC-induced matrix contraction was markedly blocked (–80%) by inhibiting the Rho-p160ROCK pathway and myosin light chain kinase, and was decreased to a lesser extent (30–40%) by a negative mutant of Rac and inhibitors of phosphatidylinositol 3-kinase (PI 3-kinase) or p38 mitogen-activated protein kinase (MAPK), but it was not affected by the inhibition of Ras and Cdc42-Wiskott-Aldrich syndrome protein (WASP) pathways. Inhibition of extracellular-signal-regulated kinase (ERK) decreased SMC-induced matrix contraction by only 15%. The migration speed and persistence of SMCs in the 3D matrix were decreased by the inhibition of p160ROCK, PI 3-kinase, p38 MAPK or WASP to different extents, and p160ROCK inhibitor had the strongest inhibitory effect. Our results suggest that the SMC-induced matrix contraction and the migration of SMCs in 3D matrix share some signaling pathways leading to force generation at cell-matrix adhesions and that various signaling pathways have different relative importance in the regulations of these processes in SMCs.


  

Author Contacts

Dr. Shu Chien
Department of Bioengineering and Whitaker Institute of Biomedical Engineering
University of California, San Diego
La Jolla, CA 92093-0427 (USA)
Tel. +1 858 534 5195, Fax +1 858 534 5453, E-Mail shuchien@ucsd.edu

  

Article Information

Received: January 24, 2003
Accepted after revision: April 23, 2003
Published online: July 29, 2003
Number of Print Pages : 11
Number of Figures : 8, Number of Tables : 0, Number of References : 66

  

Publication Details

Journal of Vascular Research (Incorporating International Journal of Microcirculation)
Founded 1964 as Angiologica by M. Comèl and L. Laszt (1964–1973) continued as Blood Vessels by J.A. Bevan (1974–1991)
Official Journal of the European Society for Microcirculation

Vol. 40, No. 4, Year 2003 (Cover Date: July-August 2003)

Journal Editor: U. Pohl, Munich
ISSN: 1018–1172 (print), 1423–0135 (Online)

For additional information: http://www.karger.com/jvr


Article / Publication Details

First-Page Preview
Abstract of Research Paper

Received: 1/24/2003
Accepted: 4/23/2003
Published online: 9/26/2003

Number of Print Pages: 11
Number of Figures: 8
Number of Tables: 0

ISSN: 1018-1172 (Print)
eISSN: 1423-0135 (Online)

For additional information: http://www.karger.com/JVR


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