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Am J Physiol Lung Cell Mol Physiol (April 12, 2002). doi:10.1152/ajplung.00459.2001
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Articles in PresS, published online ahead of print April 12, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00459.2001
Submitted on November 27, 2001
Accepted on April 5, 2002

Mechanisms of NOS2 Regulation by Rho GTPase Signaling in Airway Epithelial Cells

Nathan C. Kraynack1, Deborah A. Corey1, Heather L. Elmer1, and Thomas J. Kelley1*

1 Pediatrics, Case Western Reserve University, Cleveland, Ohio, USA

* To whom correspondence should be addressed. E-mail: tjk12{at}po.cwru.edu.

The aberrant dysregulation of the inducible form of nitric oxide synthase (NOS2) is thought to play a role in many inflammatory disorders including cystic fibrosis (CF). The complex regulation of NOS2 expression is the subject of intense investigation, and one intriguing regulatory pathway known to influence NOS2 expression is the Rho GTPase cascade. We examined NOS2 regulation in response to inflammatory cytokines in a human alveolar epithelial cell line treated with inhibitors of different upstream and downstream components of the Rho GTPase pathway in order to better define potential signaling mechanisms. Statin-mediated HMG-CoA reductase inhibition increased cytokine-dependent activation of the NOS2 promoter and was reversible by the addition of geranylgeranyl-pyrophosphate. However, inhibition of Rho associated kinase (ROCK) with Y-27632 resulted in a decrease in NOS2 promoter activity, yet an increase in NOS2 mRNA and protein levels. Our results suggest that prenylation events influence NOS2 promoter activity independently of the Rho GTPase pathway, and that Rho GTPase signaling mediated through ROCK suppresses NOS2 production downstream of promoter function at the message and protein level.




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