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1 Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, United States
2 Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, United States
3 National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, Bethesda, Maryland, United States
4 Department of Internal Medicine, University of Utah and Veterans Affairs Medical Center, Salt Lake City, Utah, United States
5 Internal Medicine, University of Utah and Veterans Affairs Medical Center, United States
6 National Institute of Diabetes and Digestive and Kidney Diseases, National Institute of Health, United States
* To whom correspondence should be addressed. E-mail: tianxin.yang{at}hsc.utah.edu.
Collecting ducts are a major site of renal production and action of both prostaglandins and nitric oxide. Experiments were undertaken to examine whether nitric oxide regulates COX-2 expression and PGE2 release in cultured collecting duct cells. In mIMCD-K2 cells sodium nitroprusside (SNP) in the 50-800 µM range induced a marked dose- and time-dependent increase in COX-2 protein levels, determined by immunoblotting, and the induction was detectable at 4 hours. This was preceded by induction of COX-2 mRNA as determined by real time-RT-PCR. The COX-2 induction was accompanied by a significant rise in PGE2 release as determined by enzyme immunoassay. S-nitroso-N-acetylpenicillamine (SNAP) had a similar stimulatory effect on COX-2 expression and PGE2 release. 8-bromo-cGMP (200 µM) had no effect on COX-2 expression. The SNP-stimulated COX-2 expression was not affected by the guanylyl cyclase inhibitor methylene blue or the protein kinase G inhibitor KT5823 (2.0 µM). In contrast, the SNP-stimulated COX-2 expression was significantly reduced by either the Erk1/2 inhibitor PD-98059 or the P38 inhibitor SB-203580, and was abolished by combination of the two kinase inhibitors. The stimulation was also significantly blocked by the SOD mimetic tempol. Thus, we conclude that NO stimulates COX-2 expression in collecting duct cells through mechanisms involving MAP kinase and superoxide, but not cGMP.
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