Cited by 345Inflammatory mediators and NSAID effectsChronic Kidney Disease and DiabetesNitric Oxide and Endothelin Effects

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Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

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Kiritoshi, Shinsuke, Nishikawa, Takeshi, Sonoda, Kazuhiro, Kukidome, Daisuke, Senokuchi, Takahumi, Matsuo, Tomoko, Matsumura, Takeshi, Tokunaga, Hiroshi, Brownlee, Michael, Araki, Eiichi·2003·Diabetes

DOI 10.2337/diabetes.52.10.2570

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Abstract

Hyperglycemia increases the production of reactive oxygen species (ROS) from the mitochondrial electron transport chain in bovine endothelial cells. Because several studies have postulated a role for prostaglandins (PGs) in the glomerular hyperfiltration seen in early diabetes, we evaluated the effect of mitochondrial ROS on expression of the inducible isoform of cyclooxygenase (COX-2) in cultured human mesangial cells (HMCs). We first confirmed that incubation of HMC with 30 mmol/l glucose significantly increased COX-2 mRNA but not COX-1 mRNA, compared with 5.6 mmol/l glucose. Similarly, incubation of HMCs with 30 mmol/l glucose significantly increased mitochondrial membrane potential, intracellular ROS production, COX-2 protein expression, and PGE2 synthesis, and these events were completely suppressed by thenoyltrifluoroacetone or carbonyl cyanide m-chlorophenylhydrazone, inhibitors of mitochondrial metabolism, or by overexpression of uncoupling protein-1 or manganese superoxide dismutase. Furthermore, increased expression of COX-2 mRNA and protein was confirmed in glomeruli of streptozotocin-induced diabetic mice. In addition, hyperglycemia induced activation of the COX-2 gene promoter, which was completely abrogated by mutation of two nuclear factor κB (NF-κB) binding sites in the promoter region. Our results suggest that hyperglycemia increases mitochondrial ROS production, resulting in NF-κB activation, COX-2 mRNA induction, COX-2 protein production, and PGE2 synthesis. This chain of events might contribute to the pathogenesis of diabetic nephropathy.

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Authors: Kiritoshi, S., Nishikawa, T., Sonoda, K., Kukidome, D., Senokuchi, T., Matsuo, T., Matsumura, T., Tokunaga, H., Brownlee, M., & Araki, E.
Affiliations: Kumamoto University (JP)
Albert Einstein College of Medicine (US)
ORCID: Nishikawa, Takeshi
Kukidome, Daisuke
Matsumura, Takeshi
Araki, Eiichi
Venue: Diabetes
Publisher: American Diabetes Association
Published: 2003-10-01
Volume: 52
Issue: 10
Pages: 2570-2577
ISSN: 0012-1797 (ISSN-L)
1939-327X
DOI: 10.2337/diabetes.52.10.2570
OpenAlex: W2468150319
Cited by: 345
References: 31
Citations by year: 2026: 5 · 2025: 6 · 2024: 7 · 2023: 8 · 2022: 18 · 2021: 12 · 2020: 8 · 2019: 12 · 2018: 10 · 2017: 11 · 2016: 15 · 2015: 14 · 2014: 20 · 2013: 16 · 2012: 26
FWCI: 9.75
Type: journal article
Language: en
Open access: bronze
doi.org
Locations: Diabetes (publishedVersion)
PubMed (publishedVersion)
Funders: Kanae Foundation for the Promotion of Medical Science
Japan Diabetes Foundation
Japan Society for the Promotion of Science (14571100)
Topics: Health Sciences › Medicine › Pharmacology (medical) › Inflammatory mediators and NSAID effects
Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
Health Sciences › Medicine › Physiology (medical) › Nitric Oxide and Endothelin Effects
Keywords: reactive oxygen species, mitochondrial reactive oxygen species, cyclooxygenase-2, mesangial cells, hyperglycemia, NF-κB, prostaglandin E2, diabetic nephropathy, glomerular hyperfiltration, UCP1, manganese superoxide dismutase, COX-2 promoter, streptozotocin-induced diabetes
MeSH terms: Uncoupling Protein 1, Animals, Carbonyl Cyanide m-Chlorophenyl Hydrazone, Carrier Proteins, Cells, Cultured, Chelating Agents, Diabetes Mellitus, Experimental, Diabetic Neuropathies, Dose-Response Relationship, Drug, Glomerular Mesangium, Glucose, Humans, Ion Channels, Ionophores, Isoenzymes, Membrane Proteins, Mitochondria, Promoter Regions, Genetic, Prostaglandin-Endoperoxide Synthases, RNA, Messenger, Superoxide Dismutase, Thenoyltrifluoroacetone, Gene Expression, Reactive Oxygen Species, Mitochondrial Proteins, Mice, Cyclooxygenase 1, Cyclooxygenase 2

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Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

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