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Identification of Intracellular Signaling Events Induced in Viable Cells by Interaction with Neighboring Cells Undergoing Apoptotic Cell Death
Published on: December 27, 2016
Inhibition of p38 mitogen-activated protein kinase phosphorylation decrease tert-butyl hydroperoxide-induced
Yuxia Yang1, Xing Liu, Jingjing Huang
1State Key Laboratory of Ophthalmology, Department of Glaucoma, Zhongshan Ophthalmic Center, Sun Yat-sen University, Guangzhou, China.
Molecular Vision
|August 10, 2012
Summary
Oxidative stress triggers apoptosis in human trabecular meshwork cells, a key factor in primary open-angle glaucoma. Inhibiting p38 mitogen-activated protein kinase (p38MAPK) protects these cells from damage.
Area of Science:
- Ophthalmology
- Cell Biology
- Biochemistry
Background:
- Oxidative stress is implicated in primary open-angle glaucoma (POAG) pathogenesis.
- Cell death in trabecular meshwork (TM) cells contributes to POAG progression.
- The precise molecular mechanisms underlying TM cell apoptosis remain unclear.
Purpose of the Study:
- To investigate the role of p38 mitogen-activated protein kinase (p38MAPK) in tert-butyl hydroperoxide (tBHP)-induced apoptosis of human trabecular meshwork (iHTM) cells.
- To elucidate the involvement of p38MAPK signaling in oxidative stress-induced TM cell death.
Main Methods:
- iHTM cells were exposed to tBHP with or without SB203580, a p38MAPK inhibitor.
- Cell viability was assessed using MTT assays.
- Reactive oxygen species (ROS) levels, proteasome activity, and apoptosis were quantified.
- Western blot analysis was used to measure phospho-p38MAPK levels.
Main Results:
- tBHP significantly increased intracellular ROS and induced apoptosis in iHTM cells.
- Pretreatment with SB203580 improved cell viability, reduced proteasome inactivation, and decreased apoptosis.
- tBHP exposure led to increased phosphorylation of p38MAPK, which was attenuated by SB203580.
Conclusions:
- Activation of p38MAPK is crucial in mediating tBHP-induced apoptosis of iHTM cells.
- Targeting p38MAPK may offer a therapeutic strategy for POAG.
- Further research into p38MAPK signaling pathways in TM cells could illuminate POAG pathogenesis.
