The cytoskeleton of arterial smooth muscle cells during human and experimental atheromatosis.
Smooth muscle cells (SMCs) implicated in the human atheromatous process show dedifferentiated features characterized by typical changes of cytoskeletal elements. In the normal media, quiescent SMCs express predominantly the alpha-smooth muscle (SM) actin isoform. In the human atheromatous plaque, and in rat experimental intimal thickening 15 days after balloon-induced endothelial injury, a decrease of the alpha-SM actin isoform and a predominance of the beta-cytoplasmic actin isoform develop. Proliferating SMCs in vivo assume fetal phenotypic features which are also observed in cultured SMCs. Thus, the study of cytoskeletal changes allows a better definition of SMC phenotype. Furthermore, in vitro SMCs may represent a useful experimental model to study phenotypic modifications of SMCs during the pathological process. Cytokines and growth factors, released by cells present in the atheromatous plaque, and extracellular components of the arterial wall, such as heparin, modulate the expression of alpha-SM actin in cultured SMCs and represent good candidates to exert important regulatory actions in vivo. A better understanding of the mechanisms leading to cytoskeletal modifications may help in the clarification of the mechanisms playing a role in the development of arterial pathological events.
Desmoulière
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A
Department of Pathology, University of Geneva, Centre Médical Universitaire, Switzerland.
Gabbiani
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G
D000199:Actins / Q000378:metabolism; D000818:Animals; D001158:Arteries / Q000378:metabolism / Q000473:pathology; D001161:Arteriosclerosis / Q000209:etiology* / Q000378:metabolism / Q000473:pathology; D002455:Cell Division; D003599:Cytoskeleton / Q000378:metabolism / Q000473:pathology*; D006801:Humans; D066298:In Vitro Techniques; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology*; D051381:Rats
D000199:Actins