ArticleMolecular vision2012
Inhibition of p38 mitogen-activated protein kinase phosphorylation decrease tert-butyl hydroperoxide-induced apoptosis in human trabecular meshwork cells.
Article in Molecular vision, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 11 citations in OpenAlex.
- The Interplay Between the Ubiquitin-Proteasome System and Oxidative Stress: A Future Perspective in Eye Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- From imbalance to impairment: the central role of reactive oxygen species in oxidative stress-induced disorders and therapeutic exploration.Frontiers in pharmacology · 2023Review
- Characterization of TGF-β by Induced Oxidative Stress in Human Trabecular Meshwork Cells.Antioxidants (Basel, Switzerland) · 2021Article
- Combining antioxidant astaxantin and cholinesterase inhibitor huperzine A boosts neuroprotection.Molecular medicine reports · 2020Article
- Article
- Inhibition of p38 mitogen-activated protein kinase phosphorylation decreases H₂O₂-induced apoptosis in human lens epithelial cells.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2015Article
- Glaucoma: an extension of various chronic neurodegenerative disorders.Molecular neurobiology · 2013Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeOxidative stress induced trabecular meshwork cells death is believed to be involved in the pathogenesis and progression of primary open-angle glaucoma (POAG). However, the intrinsic mechanism is yet to be clarified. This study is to investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in tert-butyl hydroperoxide (tBHP)-induced apoptosis of human trabecular meshwork (iHTM) cells.
methodsThe human trabecular meshwork cells were treated with tBHP for 1 or 2 h with or without pretreatment of SB203580, an inhibitor of MAP kinase homologs. Cell viability was analyzed using 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2h-tetrazolium bromide assay. Reactive oxygen species (ROS) levels were determined using dihydrodichlorofluorescein staining, and the chymotrypsin-like protease activities were measured using the Suc-LLVY-aminoluciferin substrate. Cell apoptosis was analyzed by Hoechst 33258 staining and annexin V-PI labeling. The protein level of phospho-p38 was measured using western blot analysis.
resultsThe intracellular ROS increased more than 50 fold and more than 100 fold after tBHP exposure for 1 h and 2 h, respectively (p<0.05). However, there was no difference in ROS levels between SB203580(-) and SB203580(+) cells (p>0.05). In 1 h tBHP treatment group, the cell viability was significantly improved in SB203580(+) cells (81.08%±1.93%) compared to the SB203580(-) cells (69.35%±1.52%), the chymotrypsin-like proteasome inactivation decreased in SB203580(+) cells (60.94%±0.55%) compared to the SB203580(-) cells (70.59%±0.88%), and apoptosis was impoved in SB203580(+) cells (12.75%±1.91%) compared to the SB203580(-) (28.23%±3.23%) (p<0.05). In 2 h tBHP treatment group, cell viability improved in SB203580(+) cells (76.72%±2.11%) compared to SB203580(-) cells (57.88%±2.20%), chymotrypsin-like proteasome inactivation was improved in SB203580(+) cells (62.99%±0.41%) compared to SB203580(-) cells (74.93%±0.54%), and apoptosis was improved in SB203580(+) cells (20.40%±3.44%) compared to SB203580(-) cells (39.20%±5.91%) (p<0.05). Phosphorylation of p38MAPK was significantly increased after tBHP exposure in SB203580 (-) cells and decreased sharply in SB203580(+) cells than that of control group (p<0.05). While there was no difference on the original form of p38MAPK among SB203580(-) and SB203580(+) cells after tBHP exposure and control group (p>0.05).
conclusionsActivation of p38MAPK plays an important role in tBHP-induced apoptosis of iHTM cells. Further study on the mechanisms of p38MAPK in human TM cell apoptosis may help to illuminate the pathogenesis of POAG.
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22876140PMC3413423W2097625268What OpenQuestion holds
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