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Published ahead of print on July 7, 2005, doi:10.1165/rcmb.2005-0004OC

Am. J. Respir. Cell Mol. Biol., Volume 33, Number 4, October 2005, 412-419

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Submitted on January 5, 2005
Revised on July 7, 2005

Heterotrimeric G Proteins and the PDGFR-{beta} Contribute to Hypoxic Proliferation of Smooth Muscle Cells

M. Carita Lanner1*, Maggie Raper2, Whitney M Pratt2, and Rodney A Rhoades2

1 Division of Medical Sciences, Northern Ontario School of Medicine, Sudbury, Ontario, Canada, 2 Department of Physiology, Indiana University School of Medicine, Indianapolis, Indiana, USA

* To whom correspondence should be addressed. E-mail: carita.lanner{at}normed.ca.

Hypoxic proliferation of pulmonary arterial smooth muscle cells (PASMC) is mitogen dependent, but the signaling pathways mediating hypoxia-induced cell growth are not well understood. We investigated hypoxic proliferation in primary cultures from porcine pulmonary artery smooth muscle. The cells were grown in medium with or without PDGF-B, a potent smooth muscle cell mitogen. Hypoxia induced upregulation of PDGFR-{beta} expression, the primary receptor for PDGF-B. However, PDGF-B mediated hypoxic enhancement of proliferation was abolished by pertussis toxin, indicating: 1) involvement of heterotrimeric G{alpha}i proteins and 2) minimal effect of increased PDGF receptor expression in hypoxic enhancement of proliferation. We treated PASMC with labeled, nonhydrolyzable analogues of GTP to determine directly if GTP binding proteins were activated by hypoxia in PASMC. We show that hypoxia stimulates GTP incorporation in PASMC both in the presence and absence of PDGF-B. Serum starved PASMC are able to increase their incorporation of GTP after only 10 minutes of hypoxia and this response is not pertussis toxin sensitive. In serum starved PASMC, we show that hypoxia stimulates incorporation of GTP into a 44 kDa protein. The results show that heterotrimeric G proteins are involved in hypoxia-induced signaling in pulmonary vascular smooth muscle cells.




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