ArticleThe Journal of biological chemistry2010
Protection against cytokine toxicity through endoplasmic reticulum and mitochondrial stress prevention by prostacyclin synthase overexpression in insulin-producing cells.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 24 citations in OpenAlex.
- The Potential Roles of Oral Hypoglycemic Agents to Modulate Mitochondrial Function in Type 1 Diabetes Mellitus: A Scoping Review.Life (Basel, Switzerland) · 2026Review
- PTGIS inhibited osteogenic and promoted angiogenic differentiation of bone marrow mesenchymal stem cells via endoplasmic reticulum stress mediated PI3K/AKT signaling.Stem cell research & therapy · 2026Article
- Article
- Immunometabolism in type 2 diabetes mellitus: tissue-specific interactions.Archives of medical science : AMS · 2023Article
- To Be or Not to Be: The Divergent Action and Metabolism of Sphingosine-1 Phosphate in Pancreatic Beta-Cells in Response to Cytokines and Fatty Acids.International journal of molecular sciences · 2022Review
- Identification and analysis of novel endometriosis biomarkersFrontiers in endocrinology · 2022Article
- Review
- MCPIP1 regulates the sensitivity of pancreatic beta-cells to cytokine toxicity.Cell death & disease · 2019Article
- Overexpression of sphingosine-1-phosphate lyase protects insulin-secreting cells against cytokine toxicity.The Journal of biological chemistry · 2017Article
- Regulation of pancreatic β-cell function and mass dynamics by prostaglandin signaling.Journal of cell communication and signaling · 2017Review
- Functional prostacyclin synthase promoter polymorphisms. Impact in pulmonary arterial hypertension.American journal of respiratory and critical care medicine · 2014Article
- Elevated prostacyclin biosynthesis in mice impacts memory and anxiety-like behavior.Behavioural brain research · 2014Article
- PGI2 as a regulator of inflammatory diseases.Mediators of inflammation · 2012Review
- Hypoxia upregulates PGI-synthase and increases PGI₂ release in human vascular cells exposed to inflammatory stimuli.Journal of lipid research · 2011Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Proinflammatory cytokines play a crucial role in the pathogenesis of type 1 diabetes mellitus. One of the cytokine-regulated pathways mediating inflammation in this autoimmune disease is the arachidonic acid metabolism pathway, comprising both the induction of cyclooxygenases and the production of different prostaglandins. Cytokine toxicity is mediated in many cell types, including pancreatic beta cells through this pathway. Interestingly, some cell types have been shown to be insensitive to such toxicity, and this correlated with a high expression of prostacyclin synthase (PGIS). Using insulin-producing RINm5F cells as a model for pancreatic beta cells, PGIS was overexpressed and exhibited a large protective effect against cytokine toxicity. This protective effect of PGIS against cytokine toxicity correlated with a decreased activation of the transcription factor NFkappaB and the inducible NO synthase promoter as well as a reduced inducible NO synthase protein expression and nitrite production. A reduction in the cytokine-stimulated endoplasmic reticulum and mitochondrial stress was also found in the PGIS-overexpressing cells. Moreover, cytokine-induced caspase-3 activation and reduction of glucose oxidation and cell proliferation were suppressed. Thus, PGIS overexpression apparently protects insulin-producing cells against cytokine toxicity via suppression of endoplasmic reticulum and mitochondrial stress-mediated cell death pathways.
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