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Research Database PMU-SQQUID

Matrix-degrading podosomes in smooth muscle cells.
Lener, T; Burgstaller, G; Crimaldi, L; Lach, S; Gimona, M;
Eur J Cell Biol. 2006; 85(3-4):183-189
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PMU-Authors

Gimona Mario
Lener Thomas

Abstract

Activation of protein kinase C by phorbol esters triggers the remodelling of the actin cytoskeleton and the formation of podosomes in smooth muscle cells (SMCs). Regional control of actin dynamics at specialised microdomains results in a local reduction in contractile forces. The molecular basis for this local inhibition of contractility includes the clustering of cortactin during podosome formation (which precedes the rapid, local dispersion of myosin, tropomyosin and h1 calponin), and the specific recruitment of 110-kDa actin filament-associated protein (AFAP-110) and 190-kDa Rho-specific GTPase-activating protein (p190RhoGAP) to the microdomains. Podosome formation also correlates with cell polarisation, the induction of cell motility, and local degradation of the extracellular matrix. These findings may provide explanations for the complex mechanisms underlying SMC invasion in the course of the development of atherosclerotic lesions and restenosis, and support the concept that matrix degradation and the concomitant engagement of the molecular machinery initiating actin-based cell motility drive tissue invasion in smooth muscle.


Useful keywords (using NLM MeSH Indexing)

Actin Cytoskeleton/metabolism

Actin Cytoskeleton/ultrastructure*

Animals

Cell Differentiation/physiology

Extracellular Matrix/metabolism*

Focal Adhesions/metabolism

Focal Adhesions/ultrastructure

Humans

Muscle, Smooth, Vascular/metabolism

Myocytes, Smooth Muscle/cytology

Myocytes, Smooth Muscle/metabolism*

Myocytes, Smooth Muscle/ultrastructure*

Signal Transduction/physiology

Substrate Specificity


Find related publications in this database (Keywords)

podosomes
cell motility
smooth muscle
matrix resorption
cytoskeleton
phenotypic plasticity