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2-Adrenergic receptors
increase cell migration and decrease F-actin labeling in rat aortic
smooth muscle cells
Department of Pharmacology and Toxicology, University of Arizona, Tucson, Arizona 85721-0207
Vascular wound healing and such pathologies as
atherosclerosis and restenosis are characterized by migration and
proliferation of the smooth muscle cells of the media after denudation
of the intima. To explore possible roles that
2-adrenergic receptors (2-ARs) might have in these
cellular responses, we characterized the
2-ARs present in
explant-derived cultures of rat aortic smooth muscle (RASM) cells. The
results of immunofluorescence microscopy and reverse transcription
followed by the polymerase chain reaction indicated that all three
2-AR subtypes
(2A,
2B, and
2C) were initially present.
Mitogen-activated protein kinase activity in the RASM cells was
stimulated fivefold over basal by the
2-selective agonist
dexmedetomidine (Dex) and was blocked by coincubation with the
2-selective antagonist
rauwolscine (RW) or by preincubation of the cells with the
Gi/Go-protein
inhibitor pertussis toxin. 2-AR
activation by Dex did not promote cell proliferation, as measured by
the incorporation of
[3H]thymidine.
However, Dex significantly increased RASM cell migration, and
antagonist blocked this effect. Incubation of RASM cells with Dex also
produced a marked decrease in F-actin labeling, which again was
prevented by coincubation with RW. The evidence clearly reveals the
presence of functional 2-ARs in
RASM cells. The involvement of
2-AR activation with
cytoskeletal changes and cell migration is novel and indicates a
potential role of these receptors in vascular wound healing and
pathogenesis.
atherosclerosis; G protein-coupled receptor; vascular wound healing; chemokinesis
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