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TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status
Age-related macular degeneration (AMD) is the leading cause of severe vision loss and blindness in elderly people worldwide. The damage to the retinal pigment epithelium (RPE) triggered by oxidative stress plays a central role in the onset and progression of AMD and results from the excessive accumu...
Autores principales: | , , , , , , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2023
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952053/ https://www.ncbi.nlm.nih.gov/pubmed/36829938 http://dx.doi.org/10.3390/antiox12020381 |
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author | Ramos Rego, Inês Silvério, Daniela Eufrásio, Maria Isabel Pinhanços, Sandra Sofia Lopes da Costa, Bruna Teixeira, José Fernandes, Hugo Kong, Yang Li, Yao Tsang, Stephen H. Oliveira, Paulo J. Fernandes, Rosa Quinn, Peter M. J. Santos, Paulo Fernando Ambrósio, António Francisco Alves, Celso Henrique |
author_facet | Ramos Rego, Inês Silvério, Daniela Eufrásio, Maria Isabel Pinhanços, Sandra Sofia Lopes da Costa, Bruna Teixeira, José Fernandes, Hugo Kong, Yang Li, Yao Tsang, Stephen H. Oliveira, Paulo J. Fernandes, Rosa Quinn, Peter M. J. Santos, Paulo Fernando Ambrósio, António Francisco Alves, Celso Henrique |
author_sort | Ramos Rego, Inês |
collection | PubMed |
description | Age-related macular degeneration (AMD) is the leading cause of severe vision loss and blindness in elderly people worldwide. The damage to the retinal pigment epithelium (RPE) triggered by oxidative stress plays a central role in the onset and progression of AMD and results from the excessive accumulation of reactive oxygen species (ROS) produced mainly by mitochondria. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial molecular chaperone that contributes to the maintenance of mitochondrial integrity by decreasing the production and accumulation of ROS. The present study aimed to evaluate the presence and the role of TRAP1 in the RPE. Here, we report that TRAP1 is expressed in human adult retinal pigment epithelial cells and is located mainly in the mitochondria. Exposure of RPE cells to hydrogen peroxide decreases the levels of TRAP1. Furthermore, TRAP1 silencing increases intracellular ROS production and decreases mitochondrial respiratory capacity without affecting cell proliferation. Together, these findings offer novel insights into TRAP1 functions in RPE cells, opening possibilities to develop new treatment options for AMD. |
format | Online Article Text |
id | pubmed-9952053 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2023 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-99520532023-02-25 TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status Ramos Rego, Inês Silvério, Daniela Eufrásio, Maria Isabel Pinhanços, Sandra Sofia Lopes da Costa, Bruna Teixeira, José Fernandes, Hugo Kong, Yang Li, Yao Tsang, Stephen H. Oliveira, Paulo J. Fernandes, Rosa Quinn, Peter M. J. Santos, Paulo Fernando Ambrósio, António Francisco Alves, Celso Henrique Antioxidants (Basel) Article Age-related macular degeneration (AMD) is the leading cause of severe vision loss and blindness in elderly people worldwide. The damage to the retinal pigment epithelium (RPE) triggered by oxidative stress plays a central role in the onset and progression of AMD and results from the excessive accumulation of reactive oxygen species (ROS) produced mainly by mitochondria. Tumor necrosis factor receptor-associated protein 1 (TRAP1) is a mitochondrial molecular chaperone that contributes to the maintenance of mitochondrial integrity by decreasing the production and accumulation of ROS. The present study aimed to evaluate the presence and the role of TRAP1 in the RPE. Here, we report that TRAP1 is expressed in human adult retinal pigment epithelial cells and is located mainly in the mitochondria. Exposure of RPE cells to hydrogen peroxide decreases the levels of TRAP1. Furthermore, TRAP1 silencing increases intracellular ROS production and decreases mitochondrial respiratory capacity without affecting cell proliferation. Together, these findings offer novel insights into TRAP1 functions in RPE cells, opening possibilities to develop new treatment options for AMD. MDPI 2023-02-04 /pmc/articles/PMC9952053/ /pubmed/36829938 http://dx.doi.org/10.3390/antiox12020381 Text en © 2023 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (https://creativecommons.org/licenses/by/4.0/). |
spellingShingle | Article Ramos Rego, Inês Silvério, Daniela Eufrásio, Maria Isabel Pinhanços, Sandra Sofia Lopes da Costa, Bruna Teixeira, José Fernandes, Hugo Kong, Yang Li, Yao Tsang, Stephen H. Oliveira, Paulo J. Fernandes, Rosa Quinn, Peter M. J. Santos, Paulo Fernando Ambrósio, António Francisco Alves, Celso Henrique TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title | TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title_full | TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title_fullStr | TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title_full_unstemmed | TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title_short | TRAP1 Is Expressed in Human Retinal Pigment Epithelial Cells and Is Required to Maintain their Energetic Status |
title_sort | trap1 is expressed in human retinal pigment epithelial cells and is required to maintain their energetic status |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9952053/ https://www.ncbi.nlm.nih.gov/pubmed/36829938 http://dx.doi.org/10.3390/antiox12020381 |
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