ArticleThe Journal of biological chemistry2012
Cyclooxygenase-2, not microsomal prostaglandin E synthase-1, is the mechanism for interleukin-1β-induced prostaglandin E2 production and inhibition of insulin secretion in pancreatic islets.
Article in The Journal of biological chemistry, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 39 citations in OpenAlex.
- Trial
- Article
- The Role of PGE2 in Age-related Diseases.Current drug targets · 2025Review
- Article
- Noncanonical Regulation of cAMP-Dependent Insulin Secretion and Its Implications in Type 2 Diabetes.Comprehensive Physiology · 2023Article
- Plasma Prostaglandin EMetabolites · 2022Article
- mPGES-2 blockade antagonizes β-cell senescence to ameliorate diabetes by acting on NR4A1.Nature metabolism · 2022Article
- Human Islet Expression Levels of Prostaglandin EACS pharmacology & translational science · 2021Article
- Article
- Inhibition of the prostaglandin DDiabetologia · 2020Article
- Dietary eicosapentaenoic acid normalizes hippocampal omega-3 and 6 polyunsaturated fatty acid profile, attenuates glial activation and regulates BDNF function in a rodent model of neuroinflammation induced by central interleukin-1β administration.European journal of nutrition · 2018Article
- The COX-2/PGEDiabetes · 2017Article
- Regulation of pancreatic β-cell function and mass dynamics by prostaglandin signaling.Journal of cell communication and signaling · 2017Review
- Opposing effects of prostaglandin EMolecular metabolism · 2017Article
- The PGE2 EP3 Receptor Regulates Diet-Induced Adiposity in Male Mice.Endocrinology · 2016Article
- Systemic alterations in the metabolome of diabetic NOD mice delineate increased oxidative stress accompanied by reduced inflammation and hypertriglyceremia.American journal of physiology. Endocrinology and metabolism · 2015Article
- Minireview: 12-Lipoxygenase and Islet β-Cell Dysfunction in Diabetes.Molecular endocrinology (Baltimore, Md.) · 2015Review
- Diabetes Associated Metabolomic Perturbations in NOD Mice.Metabolomics : Official journal of the Metabolomic Society · 2015Article
- Role of COX-2/mPGES-1/prostaglandin E2 cascade in kidney injury.Mediators of inflammation · 2015Review
- Comparison of the efficacy of sitagliptin and glimepiride dose-up in Japanese patients with type 2 diabetes poorly controlled by sitagliptin and glimepiride in combination.Journal of diabetes investigation · 2014Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Arachidonic acid is converted to prostaglandin E(2) (PGE(2)) by a sequential enzymatic reaction performed by two isoenzyme groups, cyclooxygenases (COX-1 and COX-2) and terminal prostaglandin E synthases (cPGES, mPGES-1, and mPGES-2). mPGES-1 is widely considered to be the final enzyme regulating COX-2-dependent PGE(2) synthesis. These generalizations have been based in most part on experiments utilizing gene expression analyses of cell lines and tumor tissue. To assess the relevance of these generalizations to a native mammalian tissue, we used isolated human and rodent pancreatic islets to examine interleukin (IL)-1β-induced PGE(2) production, because PGE(2) has been shown to mediate IL-1β inhibition of islet function. Rat islets constitutively expressed mRNAs of COX-1, COX-2, cPGES, and mPGES-1. As expected, IL-1β increased mRNA levels for COX-2 and mPGES-1, but not for COX-1 or cPGES. Basal protein levels of COX-1, cPGES, and mPGES-2 were readily detected in whole cell extracts but were not regulated by IL-1β. IL-1β increased protein levels of COX-2, but unexpectedly mPGES-1 protein levels were low and unaffected. In microsomal extracts, mPGES-1 protein was barely detectable in rat islets but clearly present in human islets; however, in neither case did IL-1β increase mPGES-1 protein levels. To further assess the importance of mPGES-1 to IL-1β regulation of an islet physiologic response, glucose-stimulated insulin secretion was examined in isolated islets of WT and mPGES-1-deficient mice. IL-1β inhibited glucose-stimulated insulin secretion equally in both WT and mPGES-1(-/-) islets, indicating that COX-2, not mPGES-1, mediates IL-1β-induced PGE(2) production and subsequent inhibition of insulin secretion.
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