ArticleMolecular vision2007
Sustained stress response after oxidative stress in trabecular meshwork cells.
Article in Molecular vision, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 69 papers.
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Who cites it
69 citing papers in PubMed, 123 citations in OpenAlex.
- Proteome cargo and functional heterogeneity of extracellular vesicles derived from stem cells and differentiated cells of human trabecular meshwork.Molecular biology reports · 2025Article
- Silencing miR-126-5p protects trabecular meshwork cells against chronic oxidative injury by upregulating HSPB8 to activate PI3K/AKT pathway.Journal of molecular histology · 2024Article
- Integrated Profiling of Extracellular Vesicle microRNA Impact on Trabecular Meshwork mRNA Expression: Insights From Microarray Analysis.Investigative ophthalmology & visual science · 2024Article
- The role of YAP/TAZ mechanosignaling in trabecular meshwork and Schlemm's canal cell dysfunction.Vision research · 2024Review
- Effects and potential mechanisms of exercise and physical activity on eye health and ocular diseases.Frontiers in medicine · 2024Review
- Distinct Metabolic Profiles of Ocular Hypertensives in Response to Hypoxia.International journal of molecular sciences · 2023Article
- Visual Impairment Risk After Alcohol Abstinence in Patients With Newly Diagnosed Open-Angle Glaucoma.JAMA network open · 2023Article
- Inflammation and retinal degenerative diseases.Neural regeneration research · 2023Review
- Mitochondrial dysfunction in glaucomatous degeneration.International journal of ophthalmology · 2023Review
- The physiological and pathophysiological roles of the autophagy lysosomal system in the conventional aqueous humor outflow pathway: More than cellular clean up.Progress in retinal and eye research · 2022Review
- Cell senescence alters responses of porcine trabecular meshwork cells to shear stress.Frontiers in cell and developmental biology · 2022Article
- Autophagy in glaucoma pathogenesis: Therapeutic potential and future perspectives.Frontiers in cell and developmental biology · 2022Review
- Baicalin suppresses glaucoma pathogenesis by regulating the PI3K/AKT signaling in vitro and in vivo.Bioengineered · 2021Article
- From Oxidative Stress to Inflammation in the Posterior Ocular Diseases: Diagnosis and Treatment.Pharmaceutics · 2021Review
- Mesenchymal stem cell-derived exosomes protect trabecular meshwork from oxidative stress.Scientific reports · 2021Article
- Article
- Low expression of GSTP1 in the aqueous humour of patients with primary open-angle glaucoma.Journal of cellular and molecular medicine · 2021Article
- Oxidative Stress and the Role of NADPH Oxidase in Glaucoma.Antioxidants (Basel, Switzerland) · 2021Review
- Nanoencapsulated hybrid compound SA-2 with long-lasting intraocular pressure-lowering activity in rodent eyes.Molecular vision · 2021Article
- Anti-inflammatory Effects of GTE in Eye Diseases.Frontiers in nutrition · 2021Review
9 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
purposeTo investigate the mechanisms by which chronic oxidative stress may lead to a sustained stress response similar to that previously observed in the trabecular meshwork (TM) of glaucoma donors.
methodsPorcine TM cells were treated with 200 microM H2O2 twice a day for four days and were allowed to recover for three additional days. After the treatment, TM cells were analyzed for generation of intracellular reactive oxygen species (iROS), mitochondrial potential, activation of NF-kappaB, and the expression of inflammatory markers IL-1alpha, IL-6, IL-8, and ELAM-1. Potential sources of iROS were evaluated using inhibitors for nitric oxide, nitric oxide synthetase, cyclooxygenase, xanthine oxidase, NADPH oxidase, mitochondrial ROS, and PKC. The role of NF-kappaB activation in the induction of inflammatory markers was evaluated using the inhibitors Lactacystin and BAY11-7082.
resultsChronic oxidative stress simulated by H2O2 exposure of porcine TM cells resulted in the sustained production of iROS by the mitochondria. Inhibition of mitochondrial iROS had a significant inhibitory effect on the activation of NF-kappaB and the induction of IL-1alpha, IL-6, IL-8, and ELAM-1 triggered by chronic oxidative stress. Inhibition of NF-kappaB partially prevented the induction of IL-1alpha, IL-8, and ELAM-1, but not IL-6.
conclusionsChronic oxidative stress in TM cells induced iROS production in mitochondria. This increase in iROS may contribute to the pathogenesis of the TM in glaucoma by inducing the expression of inflammatory mediators previously observed in glaucoma donors as well as the levels of oxidative damage in the tissue.
Indexed as
Identifiers
18199969PMC3158032W1598686935What OpenQuestion holds
Registered trials
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.