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Articles in PresS, published online ahead of print January 4, 2002
Am J Physiol Lung Cell Mol Physiol, 10.1152/ajplung.00388.2001
Submitted on October 2, 2001
Accepted on December 20, 2001
1 Medicine, University of Florida, Gainesville, FL, USA
2 Medicine, University of Florida, Gainesville, FL, USA; Research Service, Malcom Randall VA Medical Center, Gainesville, FL, USA
* To whom correspondence should be addressed. E-mail: ysu{at}ufl.edu.
The effects of specific microtubule active agents on nitric oxide (NO) production were examined in pulmonary artery endothelial cells (PAEC). PAEC were incubated with taxol, which stabilizes microtubules, or nocodazole, which disrupts microtubules, or both for 2-4 hours. We then examined NO production, endothelial nitric oxide synthase (eNOS) activity, and eNOS association with heat shock protein (Hsp90). Incubation of PAEC with taxol (15 µM) for 2-4 hours resulted in an increase in NO production, eNOS activity, and the amount of Hsp90 binding to eNOS. Incubation of PAEC with nocodazole (50 µM) for 2-4 hours induced a decrease in NO production, eNOS activity, and the amount of Hsp90 binding to eNOS. The presence of taxol in the culture medium prevented the effects of nocodazole on NO production and eNOS activity in PAEC. Geldanamycin, a Hsp90 inhibitor, prevented the taxol-induced increase in eNOS activity. Taxol and nocodazole did not affect eNOS, Hsp90, and tubulin protein contents in PAEC as detected using Western blot analysis. These results indicate that the polymerization state of the microtubule cytoskeleton regulates NO production and eNOS activity in PAEC. The changes in eNOS activity induced by modification of microtubules are due, at least in part, to the altered binding of Hsp90 to eNOS protein.
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