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Differentiation, Maintenance, and Analysis of Human Retinal Pigment Epithelium Cells: A Disease-in-a-dish Model for BEST1 Mutations
Published on: August 24, 2018
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TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status
Inês Ramos Rego1,2,3,4, Daniela Silvério1,2,3,4, Maria Isabel Eufrásio1,2,3,4
1Coimbra Institute for Clinical and Biomedical Research (iCBR), Faculty of Medicine, University Coimbra, 3000-548 Coimbra, Portugal.
Antioxidants (Basel, Switzerland)
|February 25, 2023
Summary
Tumor necrosis factor receptor-associated protein 1 (TRAP1) is present in retinal pigment epithelial cells and protects against oxidative stress. TRAP1 may offer new therapeutic targets for age-related macular degeneration (AMD).
Area of Science:
- Ophthalmology
- Cell Biology
- Mitochondrial Biology
Background:
- Age-related macular degeneration (AMD) is a leading cause of vision loss in the elderly.
- Oxidative stress and reactive oxygen species (ROS) accumulation in retinal pigment epithelium (RPE) cells contribute to AMD pathogenesis.
- Mitochondrial molecular chaperones, like TRAP1, are crucial for maintaining mitochondrial integrity and reducing ROS.
Purpose of the Study:
- To investigate the presence and function of TRAP1 in human RPE cells.
- To determine TRAP1's role in protecting RPE cells from oxidative stress.
Main Methods:
- TRAP1 expression and localization in human adult RPE cells were analyzed.
- RPE cells were exposed to hydrogen peroxide to assess TRAP1 levels.
- TRAP1 was silenced to evaluate its impact on ROS production and mitochondrial function.
Main Results:
- TRAP1 is expressed in human RPE cells and localized to mitochondria.
- Hydrogen peroxide exposure reduced TRAP1 levels in RPE cells.
- TRAP1 silencing led to increased intracellular ROS and reduced mitochondrial respiratory capacity.
Conclusions:
- TRAP1 plays a protective role in RPE cells against oxidative stress.
- TRAP1's function in RPE cells offers potential therapeutic avenues for AMD treatment.
Keywords:
age-related macular degeneration (AMD)mitochondriaoxidative stressretinal pigment epithelium (RPE)tumor necrosis factor receptor-associated protein 1 (TRAP1)
