Cargando…

Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis

Exosomes are major mediators of cell-to-cell communication, and are involved in many physiological and pathological processes. Recently, the roles of exosomes in osteoarthritis (OA) and their therapeutic potential have received increasing attention. Exosomes derived from vascular endothelial cells h...

Descripción completa

Detalles Bibliográficos
Autores principales: Yang, Run-Ze, Zheng, Huo-Liang, Xu, Wen-Ning, Zheng, Xin-Feng, Li, Bo, Jiang, Lei-Sheng, Jiang, Sheng-Dan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906201/
https://www.ncbi.nlm.nih.gov/pubmed/33526719
http://dx.doi.org/10.18632/aging.202506
_version_ 1783655246594048000
author Yang, Run-Ze
Zheng, Huo-Liang
Xu, Wen-Ning
Zheng, Xin-Feng
Li, Bo
Jiang, Lei-Sheng
Jiang, Sheng-Dan
author_facet Yang, Run-Ze
Zheng, Huo-Liang
Xu, Wen-Ning
Zheng, Xin-Feng
Li, Bo
Jiang, Lei-Sheng
Jiang, Sheng-Dan
author_sort Yang, Run-Ze
collection PubMed
description Exosomes are major mediators of cell-to-cell communication, and are involved in many physiological and pathological processes. Recently, the roles of exosomes in osteoarthritis (OA) and their therapeutic potential have received increasing attention. Exosomes derived from vascular endothelial cells have been confirmed to participate in the occurrence and development of numerous diseases; however, their effects in OA have not been reported. Here, we demonstrated the roles of exosomes secreted by vascular endothelial cells in the development of OA. Through in vivo and in vitro experiments, we demonstrated that exosomes derived from vascular endothelial cells decreased the ability of chondrocytes to resist oxidative stress by inhibiting autophagy and p21 expression, thereby increasing the cellular ROS content and inducing apoptosis. These findings indicate that exosomes derived from vascular endothelial cells promote the progression of OA, thus, providing new ideas for the diagnosis and treatment of OA.
format Online
Article
Text
id pubmed-7906201
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Impact Journals
record_format MEDLINE/PubMed
spelling pubmed-79062012021-03-04 Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis Yang, Run-Ze Zheng, Huo-Liang Xu, Wen-Ning Zheng, Xin-Feng Li, Bo Jiang, Lei-Sheng Jiang, Sheng-Dan Aging (Albany NY) Research Paper Exosomes are major mediators of cell-to-cell communication, and are involved in many physiological and pathological processes. Recently, the roles of exosomes in osteoarthritis (OA) and their therapeutic potential have received increasing attention. Exosomes derived from vascular endothelial cells have been confirmed to participate in the occurrence and development of numerous diseases; however, their effects in OA have not been reported. Here, we demonstrated the roles of exosomes secreted by vascular endothelial cells in the development of OA. Through in vivo and in vitro experiments, we demonstrated that exosomes derived from vascular endothelial cells decreased the ability of chondrocytes to resist oxidative stress by inhibiting autophagy and p21 expression, thereby increasing the cellular ROS content and inducing apoptosis. These findings indicate that exosomes derived from vascular endothelial cells promote the progression of OA, thus, providing new ideas for the diagnosis and treatment of OA. Impact Journals 2021-02-01 /pmc/articles/PMC7906201/ /pubmed/33526719 http://dx.doi.org/10.18632/aging.202506 Text en Copyright: © 2021 Yang et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Yang, Run-Ze
Zheng, Huo-Liang
Xu, Wen-Ning
Zheng, Xin-Feng
Li, Bo
Jiang, Lei-Sheng
Jiang, Sheng-Dan
Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title_full Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title_fullStr Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title_full_unstemmed Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title_short Vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
title_sort vascular endothelial cell-secreted exosomes facilitate osteoarthritis pathogenesis by promoting chondrocyte apoptosis
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7906201/
https://www.ncbi.nlm.nih.gov/pubmed/33526719
http://dx.doi.org/10.18632/aging.202506
work_keys_str_mv AT yangrunze vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT zhenghuoliang vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT xuwenning vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT zhengxinfeng vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT libo vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT jiangleisheng vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis
AT jiangshengdan vascularendothelialcellsecretedexosomesfacilitateosteoarthritispathogenesisbypromotingchondrocyteapoptosis