Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria

Abstract Temporomandibular joint osteoarthritis (TMJOA) urgently needs regenerative therapies due to the limited effects of traditional treatments. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) are considered a potent alternative for MSC therapy for the treatment of TMJOA. However,...

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Main Authors: Ziyi Mei, Hanyue Li, Chuling Huang, Shiyong Ma, Yuejia Li, Pingmeng Deng, Sha Zhou, Aizhuo Qian, Bin Yang, Jie Li
Format: Article
Language:English
Published: BMC 2025-05-01
Series:Journal of Nanobiotechnology
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Online Access:https://doi.org/10.1186/s12951-025-03478-9
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author Ziyi Mei
Hanyue Li
Chuling Huang
Shiyong Ma
Yuejia Li
Pingmeng Deng
Sha Zhou
Aizhuo Qian
Bin Yang
Jie Li
author_facet Ziyi Mei
Hanyue Li
Chuling Huang
Shiyong Ma
Yuejia Li
Pingmeng Deng
Sha Zhou
Aizhuo Qian
Bin Yang
Jie Li
author_sort Ziyi Mei
collection DOAJ
description Abstract Temporomandibular joint osteoarthritis (TMJOA) urgently needs regenerative therapies due to the limited effects of traditional treatments. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) are considered a potent alternative for MSC therapy for the treatment of TMJOA. However, the specific mechanisms remain inadequately investigated. In this study, we explored how EVs from adipose-derived stromal/stem cells (ASCs) influence the TMJOA model triggered by Complete Freund’s Adjuvant in rats and their impact on the state of dendritic cells (DCs) under pathological conditions. Subsequently, we conducted transcriptomic and metabolomic analyses to elucidate the specific mechanisms by which EVs affect DCs. Mechanistically, we demonstrate that EVs transferred functional mitochondria to DCs, which reverses their metabolic states. The internalized functional mitochondria from EVs activate the MAPK/ERK1/2/FoxO1/autophagy pathway, which causes the metabolic reprogramming of DCs and facilitates the achievement of therapeutic effects. These findings provide a mechanistic rationale for utilizing ASCs-EVs as cell-free alternatives to MSC transplantation in TMJOA therapy. Graphical Abstract
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institution OA Journals
issn 1477-3155
language English
publishDate 2025-05-01
publisher BMC
record_format Article
series Journal of Nanobiotechnology
spelling doaj-art-582dbc7edfb24592bc8c7f3ce2faebe92025-08-20T02:03:39ZengBMCJournal of Nanobiotechnology1477-31552025-05-0123112010.1186/s12951-025-03478-9Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondriaZiyi Mei0Hanyue Li1Chuling Huang2Shiyong Ma3Yuejia Li4Pingmeng Deng5Sha Zhou6Aizhuo Qian7Bin Yang8Jie Li9College of Stomatology, Chongqing Medical UniversityDepartment of Stomatology, Shenzhen Hospital, Southern Medical UniversityCollege of Stomatology, Chongqing Medical UniversityBasic Medicine Research and Innovation Center for Novel Target and Therapeutic Intervention, The Ministry of Education, College of Pharmacy, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityCollege of Stomatology, Chongqing Medical UniversityAbstract Temporomandibular joint osteoarthritis (TMJOA) urgently needs regenerative therapies due to the limited effects of traditional treatments. Mesenchymal stem cell-derived extracellular vesicles (MSC-EVs) are considered a potent alternative for MSC therapy for the treatment of TMJOA. However, the specific mechanisms remain inadequately investigated. In this study, we explored how EVs from adipose-derived stromal/stem cells (ASCs) influence the TMJOA model triggered by Complete Freund’s Adjuvant in rats and their impact on the state of dendritic cells (DCs) under pathological conditions. Subsequently, we conducted transcriptomic and metabolomic analyses to elucidate the specific mechanisms by which EVs affect DCs. Mechanistically, we demonstrate that EVs transferred functional mitochondria to DCs, which reverses their metabolic states. The internalized functional mitochondria from EVs activate the MAPK/ERK1/2/FoxO1/autophagy pathway, which causes the metabolic reprogramming of DCs and facilitates the achievement of therapeutic effects. These findings provide a mechanistic rationale for utilizing ASCs-EVs as cell-free alternatives to MSC transplantation in TMJOA therapy. Graphical Abstracthttps://doi.org/10.1186/s12951-025-03478-9Extracellular vesiclesMitochondriaDendritic cellsAutophagyReprogramming metabolism
spellingShingle Ziyi Mei
Hanyue Li
Chuling Huang
Shiyong Ma
Yuejia Li
Pingmeng Deng
Sha Zhou
Aizhuo Qian
Bin Yang
Jie Li
Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
Journal of Nanobiotechnology
Extracellular vesicles
Mitochondria
Dendritic cells
Autophagy
Reprogramming metabolism
title Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
title_full Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
title_fullStr Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
title_full_unstemmed Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
title_short Extracellular vesicles from adipose-derived stromal/stem cells reprogram dendritic cells to alleviate rat TMJOA by transferring mitochondria
title_sort extracellular vesicles from adipose derived stromal stem cells reprogram dendritic cells to alleviate rat tmjoa by transferring mitochondria
topic Extracellular vesicles
Mitochondria
Dendritic cells
Autophagy
Reprogramming metabolism
url https://doi.org/10.1186/s12951-025-03478-9
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