ArticleProceedings of the National Academy of Sciences of the United States of America1998
Basal expression of cyclooxygenase-2 and nuclear factor-interleukin 6 are dominant and coordinately regulated by interleukin 1 in the pancreatic islet.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
36 citing papers in PubMed, 140 citations in OpenAlex.
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- Distinct etiology of chronic inflammation - implications on degenerative diseases and cancer therapy.Frontiers in immunology · 2024Review
- Human Islet Expression Levels of Prostaglandin EACS pharmacology & translational science · 2021Article
- COX-2 Is Downregulated in Human Stenotic Aortic Valves and Its Inhibition Promotes Dystrophic Calcification.International journal of molecular sciences · 2020Article
- Inhibition of the prostaglandin DDiabetologia · 2020Article
- Prostaglandins in asthma and allergic diseases.Pharmacology & therapeutics · 2019Review
- PLK2 Plays an Essential Role in High D-Glucose-Induced Apoptosis, ROS Generation and Inflammation in Podocytes.Scientific reports · 2017Article
- Regulation of pancreatic β-cell function and mass dynamics by prostaglandin signaling.Journal of cell communication and signaling · 2017Review
- Dietary polyunsaturated fatty acids and their metabolites: Implications for diabetes pathophysiology, prevention, and treatment.Nutrition and healthy aging · 2017Review
- Effective suppression of pro-inflammatory molecules by DHCA via IKK-NF-κB pathway, in vitro and in vivo.British journal of pharmacology · 2015Article
- Inhibition of IκB kinase (IKK) protects against peripheral nerve dysfunction of experimental diabetes.Molecular neurobiology · 2015Article
- The role of prostaglandins in allergic lung inflammation and asthma.Expert review of respiratory medicine · 2015Review
- Group X secretory phospholipase A2 regulates insulin secretion through a cyclooxygenase-2-dependent mechanism.The Journal of biological chemistry · 2014Article
- Inhibitory G proteins and their receptors: emerging therapeutic targets for obesity and diabetes.Experimental & molecular medicine · 2014Review
- Pro-inflammatory and pro-oxidant status of pancreatic islet in vitro is controlled by TLR-4 and HO-1 pathways.PloS one · 2014Article
- 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.The Journal of biological chemistry · 2012Article
- Expression of cyclooxygenase-1 (COX-1) and COX-2 in human male gametes from normal patients, and those with varicocele and diabetes: a potential molecular marker for diagnosing male infertility disorders.Journal of anatomy · 2012Article
- PTGS-2-PTGER2/4 signaling pathway partially protects from diabetogenic toxicity of streptozotocin in mice.Diabetes · 2012Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
The enzyme cyclooxygenase (COX)-1 is constitutive whereas COX-2 is regulated in virtually all tissues. To assess whether this dogma holds true in the pancreatic islet, we examined basal and interleukin (IL)-1-regulated expression of COX-2 in HIT-T15 cells, Syrian hamster and human islets, and other Syrian hamster tissues. We found that COX-2, and not COX-1, gene expression is dominant in pancreatic islet tissue under both basal and IL-1-stimulated conditions. Control tissues (liver, spleen, and kidney) showed the expected predominance of COX-1 gene expression. Basal and IL-1-stimulated prostaglandin E2 synthesis were blocked by a specific COX-2 inhibitor. IL-1 stimulation had a biphasic effect on COX-2 mRNA levels with an initial mild increase at 2-4 hr followed by a more dramatic decrease below basal level by 24 hr. The IL-1-induced increase in COX-2 mRNA levels was accompanied by a parallel increase in NF-kappaB binding to COX-2 promoter elements. The subsequent decrease in COX-2 mRNA levels was accompanied by a parallel decrease in NF-IL-6 binding activity and COX-2 promoter activity. Specific mutation of the NF-IL-6 binding motif within the COX-2 promoter reduced basal promoter activity by 50% whereas mutation of the NF-kappaB motif had no effect. These studies provide documentation of NF-IL-6 in the pancreatic islet and that COX-2, rather than COX-1, is dominantly expressed. They suggest coordinate regulation by IL-1 of COX-2 mRNA, NF-kappaB, and NF-IL-6 and raise the issue of whether intrinsically high levels of COX-2 gene expression predisposes the normal islet for microenvironmentally induced overproduction of islet prostaglandin E2.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.