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Published ahead of print on July 15, 2004, doi:10.1165/rcmb.2003-0426OC

Am. J. Respir. Cell Mol. Biol., Volume 31, Number 5, November 2004, 544-551

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Submitted on November 25, 2003
Revised on July 13, 2004

Cobalt induces HIF-1{alpha} expression in ASM cells by a ROS and PI3K dependent mechanism

Georgia Chachami1, George Simos2, Apostolia Hatziefthimiou3, Sophia Bonanou2, Paschalis-Adam Molyvdas3, and Efrosyni Paraskeva3*

1 Department of Medicine, Laboratory of Physiology, University of Thessaly, School of Health Sciences, Larissa, Greece; Department of Medicine, Laboratory of Biochemistry, University of Thessaly, School of Health Sciences, Larissa, Greece, 2 Department of Medicine, Laboratory of Biochemistry, University of Thessaly, School of Health Sciences, Larissa, Greece, 3 Department of Medicine, Laboratory of Physiology, University of Thessaly, School of Health Sciences, Larissa, Greece

* To whom correspondence should be addressed. E-mail: fparaskeva{at}med.uth.gr.

Cobalt can mimic hypoxia and has been incriminated for causing lung defects. However, the effect of cobalt on airway smooth muscle (ASM) cells has not been analyzed in detail. In this report we use primary cultures of ASM cells from rabbit trachea and show that exposure to CoCl2 causes a rapid increase of the intracellular levels of the hypoxia inducible factor HIF-1{alpha}, which is detected predominantly inside the nucleus. With the use of specific inhibitors we demonstrate that induction of HIF-1{alpha} by cobalt depends on active protein synthesis but not transcription. Furthermore, wortmannin, LY294002 and N-acetyl-L-cysteine inhibit the effect of cobalt suggesting that it involves the phosphatidylinositol 3-kinase pathway and production of reactive oxygen species. Interestingly CoCl2 attenuates the contractile response of rabbit airways induced by KCl, but not by acetylcholine, suggesting a link between the cellular response to hypoxic stimuli and the contractile properties of ASM cells.




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