Cytokine-induced PGE2 formation is reduced from iNOS deficient murine islets
Autor: | Annika K. Andersson, Carina Carlsson, Lina Thorvaldson, Stellan Sandler |
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Rok vydání: | 2004 |
Předmět: |
endocrine system
medicine.medical_specialty Cell Survival medicine.medical_treatment Nitric Oxide Synthase Type II Stimulation Nitric Oxide Biochemistry Dinoprostone Nitric oxide Interferon-gamma Islets of Langerhans Mice chemistry.chemical_compound Endocrinology Internal medicine Insulin Secretion medicine Animals Insulin RNA Messenger Molecular Biology Cells Cultured Mice Knockout chemistry.chemical_classification Messenger RNA geography geography.geographical_feature_category biology Islet Isoenzymes Nitric oxide synthase Cytokine Enzyme chemistry Cyclooxygenase 2 Prostaglandin-Endoperoxide Synthases biology.protein Nitric Oxide Synthase Gene Deletion Interleukin-1 Prostaglandin E |
Zdroj: | Molecular and Cellular Endocrinology. 220:21-29 |
ISSN: | 0303-7207 |
Popis: | Cytokines may be involved in islet destruction during Type 1 diabetes. Exposure to interleukin-1beta (IL-1beta) or IL-1beta plus interferon-gamma (IFN-gamma) of rodent islets induces expression of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Subsequent formation of nitric oxide (NO) and prostaglandin E(2) (PGE(2)) may impair beta-cell function. Using iNOS deficient (iNOS -/-) islets, we have further investigated the relation between NO formation and PGE(2) induction. We found that iNOS -/- islets responded with a reduced PGE(2) formation following IL-1beta or (IL-1beta + IFN-gamma) treatment compared to wild-type (wt) islets, while COX-2 mRNA or protein content were unchanged. By the addition of an NO donor together with IL-1beta, PGE(2) formation could be stimulated from iNOS -/- islets. We conclude that the lowered capacity of PGE(2) formation observed from cytokine exposed iNOS -/- islets is due to a decreased stimulation of PGE(2) formation by the COX-2 enzyme in the absence of NO, rather then differences in expressed COX-2 protein. |
Databáze: | OpenAIRE |
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