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Acta Biochimica et Biophysica Sinica 2005 37(2):139-146; doi:10.1093/abbs/37.2.139
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© 2005 Institute of Biochemistry and Cell Biology, SIBS, CAS

Potential Role of NO in Modulation of COX-2 Expression and PGE2 Production in Pancreatic β-cells

Jia-Jian Ling, Yu-Jie Sun, Dong-Ya Zhu1, Qi Chen and Xiao Han*

The Key Laboratory of Human Functional Genomics of Jiangsu Province, Nanjing Medical University Nanjing 210029, China
1 School of Pharmacy, Nanjing Medical University Nanjing 210029, China

Edited by Chong-Rong Sun

* Corresponding author: Tel, 86-25-86862731/86862733; E-mail, hanxiao{at}njmu.edu.cn


  Abstract

Cytokines have been implicated in pancreatic β-cell destruction leading to type 1 diabetes. Exposure to interleukin-1β (IL-1β) of pancreatic β-cells induces expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Subsequent formation of nitric oxide (NO) and prostaglandin E2 (PGE2) may impair β-cell function. Using NOS inhibitor NG-monomethyl-L-arginine (L-NMMA), we have further investigated the relation between NO formation and COX-2 expression. IL-1β stimulated the formation of NO and PGE2 by pancreatic β-cells. L-NMMA completely inhibited IL-1β-induced NO formation and attenuated PGE2 production. COX-2 gene transcription level and protein expression were determined by real-time PCR, Western blot and luciferase analysis. L-NMMA inhibited IL-1β-induced promoter activity, gene transcription and protein expression of COX-2 in pancreatic β-cells. Therefore, we concluded that NO-affected COX-2 activity is directly linked to COX-2 gene transcription and protein expression in pancreatic β-cells. The identification of a novel interaction of NO on the COX signaling pathway in β-cells provides a strategy of intervention for further evaluating the role of NO and PGE2 in autoimmune diabetes.

Keywords    nitric oxide; cyclooxygenase-2; pancreatic β-cell; prostaglandin E2

Received: October 27, 2004; Accepted: January 7, 2005
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