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1 Department of Cellular and Molecular Medicine, Kidney Research Center, Faculty of Medicine, University of Ottawa, Ottawa, ON, Canada
* To whom correspondence should be addressed. E-mail: rlhebert{at}uottawa.ca.
Alterations in renal prostaglandins may contribute to some of the renal manifestations in diabetes leading to nephropathy. Prostaglandin production is dependent upon the activity of cyclooxygenases (COX-1 AND -2) and prostaglandin synthases. Our current study has investigated levels of these enzymes in rat streptozotocin-diabetes at 2, 4, 6 and 8 weeks of diabetes. Immunohistochemical analysis revealed an increase in COX signal in the inner and outer medulla of the diabetic rats. This was confirmed by Western blotting, showing up to a 4 -fold increase in both COX isoforms at 4-6 weeks of diabetes. Also, Western blot analysis revealed a 6-fold increase in PGE2 synthase expression in the outer medullary region of 6 weeks diabetic rats, but no difference in the inner medulla. In cultured rat IMCD, levels of COX were increased 2-3 -fold in cells exposed for 4 days to 37.5 mM glucose in comparison to control of 17.5 mM. While no change in PGE2 synthase levels was noted, PGE2 synthesis was increased. Furthermore, levels of EP1 and EP4 mRNA were increased, as well as a 2 -fold increase in EP4 protein levels. Future studies will determine which COX isoform is contributing to the majority of PGE2 produced in the diabetic IMCD, and the significance of these findings to disturbances in IMCD function and to the progression of diabetic nephropathy.
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