TITLE

Regulation of Human Vascular Smooth Muscle Cell Migration by β-Adrenergic Receptors

AUTHOR(S)
Johnson, Richard; Webb, Jerry G.; Newman, Walter H.; Zhongbiao Wang
PUB. DATE
January 2006
SOURCE
American Surgeon;Jan2006, Vol. 72 Issue 1, p51
SOURCE TYPE
Academic Journal
DOC. TYPE
Article
ABSTRACT
Migration and proliferation of vascular smooth muscle cells (VSMCs) are two events involved in atherosclerosis, restenosis after balloon angioplasty, and stenosis of grafted vessels. Platelet-derived growth factor (PDGF) found in stenotic vessels is known to induce migration of VSMCs. VSMCs express both α and β-adrenergic receptors on their surface, and blood vessels are innervated by the adrenergic nervous system and exposed to circulating epinephrine. We examined the role of these receptors on PDGF-induced migration of VSMCs. VSMCs were cultured from saphenous vein segments. Migration was stimulated by PDGF. Effect of pretreatment of VSMCs with the p-agonist isoproterenol, the a-agonist phenylephrine, or forskolin on PDGF-induced migration was examined with a modified Boyden chamber. Cell migration was quantitated by spectrophotometry. Intracellular cyclic AMP was determined by radioimmunoassay. PDGF significantly induced VSMC migration. Isoproterenol (0.1 and 1.0 µM) inhibited PDGF-induced migration by 30 per cent and 50 per cent, respectively. Forskolin (10 µM) completely blocked PDGF-induced migration. The migration inhibition by isoproterenol or forskolin was associated with a significant elevation of intracellular cyclic AMP. In contrast, phenylephrine had no effect on PDGF-induced migration or on cyclic AMP. Activation of P-adrenergic receptors and the consequent rise in intracellular cyclic AMP inhibits migration of VSMCs induced by PDGF. These results are consistent with the notion that adrenergic agonists with substantial β-receptor affinity, such as isoproterenol, can inhibit smooth muscle cell migration.
ACCESSION #
19500441

 

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