BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization

Abstract Osteoporosis is characterized by reduced bone mass due to imbalanced bone metabolism. Exosomes derived from bone mesenchymal stem cells (BMSCs) have been shown to play roles in various diseases. This study aimed to clarify the regulatory function and molecular mechanism of BMSCs-derived exo...

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Main Authors: Yanbin Zhang, Jing Bai, Bin Xiao, Chunyan Li
Format: Article
Language:English
Published: BMC 2024-11-01
Series:Molecular Medicine
Subjects:
Online Access:https://doi.org/10.1186/s10020-024-00904-w
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author Yanbin Zhang
Jing Bai
Bin Xiao
Chunyan Li
author_facet Yanbin Zhang
Jing Bai
Bin Xiao
Chunyan Li
author_sort Yanbin Zhang
collection DOAJ
description Abstract Osteoporosis is characterized by reduced bone mass due to imbalanced bone metabolism. Exosomes derived from bone mesenchymal stem cells (BMSCs) have been shown to play roles in various diseases. This study aimed to clarify the regulatory function and molecular mechanism of BMSCs-derived exosomes in osteogenic differentiation and their potential therapeutic effects on osteoporosis. Exosomes were extracted from BMSCs. Bone marrow-derived macrophages (BMDMs) were cultured and internalized with BMSCs-derived exosomes. Real-time quantitative PCR was used to detect the expression of macrophage surface markers and tripartite motif (TRIM) family genes. BMDMs were co-cultured with human osteoblasts to assess osteogenic differentiation. Western blot was performed to analyze the ubiquitination of triggering receptor expressed on myeloid cell 1 (TREM1) mediated by TRIM25. An ovariectomized mice model was established to evaluate the role of TRIM25 and exosomes in osteoporosis. Exosomes were successfully isolated from BMSCs. BMSCs-derived exosomes upregulated TRIM25 expression, promoting M2 macrophage polarization and osteogenic differentiation. TRIM25 facilitated the ubiquitination and degradation of TREM1. Overexpression of TREM1 reversed the enhanced M2 macrophage polarization and osteogenic differentiation caused by TRIM25 overexpression. TRIM25 enhanced the protective effect of BMSCs-derived exosomes against bone loss in mice. These findings suggested that BMSCs-derived exosomes promoted osteogenic differentiation by regulating M2 macrophage polarization through TRIM25-mediated ubiquitination and degradation of TREM1. This mechanism might provide a novel approach for treating osteoporosis.
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spelling doaj-art-db2dc6714c164d7d850b248e058952ec2025-08-20T01:47:29ZengBMCMolecular Medicine1528-36582024-11-0130111610.1186/s10020-024-00904-wBMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarizationYanbin Zhang0Jing Bai1Bin Xiao2Chunyan Li3Department of Spine Surgery, National Center for Orthopaedics, Capital Medical University Affiliated Beijing Jishuitan HospitalDepartment of Trauma and Joint, The Third Affiliated Hospital of Beijing University of Traditional Chinese MedicineDepartment of Spine Surgery, National Center for Orthopaedics, Capital Medical University Affiliated Beijing Jishuitan HospitalDepartment of Clinial Laboratory, Capital Medical University Affiliated Beijing Jishuitan HospitalAbstract Osteoporosis is characterized by reduced bone mass due to imbalanced bone metabolism. Exosomes derived from bone mesenchymal stem cells (BMSCs) have been shown to play roles in various diseases. This study aimed to clarify the regulatory function and molecular mechanism of BMSCs-derived exosomes in osteogenic differentiation and their potential therapeutic effects on osteoporosis. Exosomes were extracted from BMSCs. Bone marrow-derived macrophages (BMDMs) were cultured and internalized with BMSCs-derived exosomes. Real-time quantitative PCR was used to detect the expression of macrophage surface markers and tripartite motif (TRIM) family genes. BMDMs were co-cultured with human osteoblasts to assess osteogenic differentiation. Western blot was performed to analyze the ubiquitination of triggering receptor expressed on myeloid cell 1 (TREM1) mediated by TRIM25. An ovariectomized mice model was established to evaluate the role of TRIM25 and exosomes in osteoporosis. Exosomes were successfully isolated from BMSCs. BMSCs-derived exosomes upregulated TRIM25 expression, promoting M2 macrophage polarization and osteogenic differentiation. TRIM25 facilitated the ubiquitination and degradation of TREM1. Overexpression of TREM1 reversed the enhanced M2 macrophage polarization and osteogenic differentiation caused by TRIM25 overexpression. TRIM25 enhanced the protective effect of BMSCs-derived exosomes against bone loss in mice. These findings suggested that BMSCs-derived exosomes promoted osteogenic differentiation by regulating M2 macrophage polarization through TRIM25-mediated ubiquitination and degradation of TREM1. This mechanism might provide a novel approach for treating osteoporosis.https://doi.org/10.1186/s10020-024-00904-wExosomeBone mesenchymal stem cellsPolarizationTRIM25TREM1Ubiquitination
spellingShingle Yanbin Zhang
Jing Bai
Bin Xiao
Chunyan Li
BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
Molecular Medicine
Exosome
Bone mesenchymal stem cells
Polarization
TRIM25
TREM1
Ubiquitination
title BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
title_full BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
title_fullStr BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
title_full_unstemmed BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
title_short BMSC-derived exosomes promote osteoporosis alleviation via M2 macrophage polarization
title_sort bmsc derived exosomes promote osteoporosis alleviation via m2 macrophage polarization
topic Exosome
Bone mesenchymal stem cells
Polarization
TRIM25
TREM1
Ubiquitination
url https://doi.org/10.1186/s10020-024-00904-w
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AT jingbai bmscderivedexosomespromoteosteoporosisalleviationviam2macrophagepolarization
AT binxiao bmscderivedexosomespromoteosteoporosisalleviationviam2macrophagepolarization
AT chunyanli bmscderivedexosomespromoteosteoporosisalleviationviam2macrophagepolarization