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Published ahead of print on January 31, 2003, doi:10.1165/rcmb.2002-0254OC

Am. J. Respir. Cell Mol. Biol., Volume 29, Number 1, July 2003, 19-27

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Submitted on November 14, 2002
Revised on January 30, 2003

Cyclic AMP-Mobilizing Agents and Glucocorticoids Modulate Human Smooth Muscle Cell Migration

Elena A Goncharova1, Charlotte K Billington2, Carla Irani1, Alexander V Vorotnikov3, Vsevolod A Tkachuk3, Raymond B Penn2, Vera P Krymskaya1, and Reynold A Panettieri, Jr.1*

1 Medicine, University of Pennsylvania, Philadelphia, PA, USA, 2 Division of Critical Care, Pulmonary, Allergic and Immunological Diseases, Kimmel Cancer Center, Thomas Jefferson University, Philadelphia, PA, USA, 3 Institute of Experimental Cardiology, Russian Cardiology research center, Moscow, Russian Federation

* To whom correspondence should be addressed. E-mail: RAP{at}mail.med.upenn.edu.

Hyperplasia and cell migration of smooth muscle are features of both airway and pulmonary vascular diseases. The precise cellular and molecular mechanisms that regulate smooth muscle migration in the lungs remain unknown. In this study, we examined the effect of cAMP-mobilizing agents and steroids on smooth muscle cell migration. PDGF, TGF{alpha}, VEGF, and bFGF significantly stimulated cell migration in PVSM cells. ASM migration was also stimulated by PDGF, TGF{alpha}, and bFGF but VEGF was without effect. Interestingly, the smooth muscle mitogen thrombin did not stimulate migration of either cell type. Agents capable of elevating intracellular cAMP inhibited basal (unstimulated) cell migration in both cell types, whereas their effects on PDGF-stimulated migration were more variable. PGE2, salmeterol, and the phosphodiesterase type 4 inhibitor cilomolast inhibited basal ASM and PVSM migration by 30-60%. PGE2 and cilomolast also inhibited PDGF-stimulated migration of ASM and PVSM cells but salmeterol was without effect. Preincubation of ASM cells with dexamethasone or fluticasone inhibited basal and PDGF-stimulated migration, and enabled an inhibitory effect of salmeterol on PDGF-induced cell migration. Steroids alone did not stimulate cAMP production or cAMP/PKA-dependent gene transcription (CRE-Luc activity), but slightly augmented salmeterol-stimulated CRE-Luc activity. Collectively, these findings demonstrate that cAMP-mobilizing agents and steroids modulate human smooth muscle cell migration, likely by distinct mechanisms.




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