Aged bone matrix-derived extracellular vesicles as a messenger for calcification paradox

Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification parado...

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Published inNature communications Vol. 13; no. 1; pp. 1453 - 20
Main Authors Wang, Zhen-Xing, Luo, Zhong-Wei, Li, Fu-Xing-Zi, Cao, Jia, Rao, Shan-Shan, Liu, Yi-Wei, Wang, Yi-Yi, Zhu, Guo-Qiang, Gong, Jiang-Shan, Zou, Jing-Tao, Wang, Qiang, Tan, Yi-Juan, Zhang, Yan, Hu, Yin, Li, You-You, Yin, Hao, Wang, Xiao-Kai, He, Ze-Hui, Ren, Lu, Liu, Zheng-Zhao, Hu, Xiong-Ke, Yuan, Ling-Qing, Xu, Ran, Chen, Chun-Yuan, Xie, Hui
Format Journal Article
LanguageEnglish
Published London Nature Publishing Group UK 18.03.2022
Nature Publishing Group
Nature Portfolio
Subjects
49/61
64/110
64/60
692/163/2743/316/801
692/4019/592/2193
692/698/1671/63
Adipogenesis
Adipose tissue
Aging
Alendronic acid
Animals
Biomedical materials
Bisphosphonates
Bone marrow
Bone Matrix
Bone resorption
Calcification
Calcification (ectopic)
Cell Differentiation
Extracellular Vesicles
Female
Humanities and Social Sciences
Intravenous administration
Matrix vesicles
Menopause
Mesenchymal Stem Cells
Mesenchyme
Mice
MicroRNAs - genetics
multidisciplinary
Muscles
Oophorectomy
Osteoblastogenesis
Osteogenesis
Osteoporosis
Ovariectomy
Paradoxes
Science
Science (multidisciplinary)
Smooth muscle
Stromal cells
Vesicles
Vitamin D3
Online AccessGet full text

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Abstract Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861. This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification (calcification paradox) during skeletal aging and menopause by transferring miR-483-5p and miR-2861.
AbstractList Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861.
Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861. This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification (calcification paradox) during skeletal aging and menopause by transferring miR-483-5p and miR-2861.
Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called "calcification paradox". Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861.Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called "calcification paradox". Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861.
Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related marrow adiposity and osteoporosis. Vascular calcification often occurs with osteoporosis, a contradictory association called “calcification paradox”. Here we show that extracellular vesicles derived from aged bone matrix (AB-EVs) during bone resorption favor BMSC adipogenesis rather than osteogenesis and augment calcification of vascular smooth muscle cells. Intravenous or intramedullary injection of AB-EVs promotes bone-fat imbalance and exacerbates Vitamin D3 (VD3)-induced vascular calcification in young or old mice. Alendronate (ALE), a bone resorption inhibitor, down-regulates AB-EVs release and attenuates aging- and ovariectomy-induced bone-fat imbalance. In the VD3-treated aged mice, ALE suppresses the ovariectomy-induced aggravation of vascular calcification. MiR-483-5p and miR-2861 are enriched in AB-EVs and essential for the AB-EVs-induced bone-fat imbalance and exacerbation of vascular calcification. Our study uncovers the role of AB-EVs as a messenger for calcification paradox by transferring miR-483-5p and miR-2861.This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification (calcification paradox) during skeletal aging and menopause by transferring miR-483-5p and miR-2861.
This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification (calcification paradox) during skeletal aging and menopause by transferring miR-483-5p and miR-2861.
ArticleNumber 1453
Author Zou, Jing-Tao
Rao, Shan-Shan
Liu, Yi-Wei
Xu, Ran
Wang, Qiang
Cao, Jia
Yuan, Ling-Qing
Li, Fu-Xing-Zi
Hu, Xiong-Ke
Zhang, Yan
Hu, Yin
Xie, Hui
Gong, Jiang-Shan
Yin, Hao
Ren, Lu
Liu, Zheng-Zhao
Wang, Xiao-Kai
Wang, Yi-Yi
Li, You-You
Chen, Chun-Yuan
He, Ze-Hui
Zhu, Guo-Qiang
Wang, Zhen-Xing
Luo, Zhong-Wei
Tan, Yi-Juan
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– sequence: 2
  givenname: Zhong-Wei
  surname: Luo
  fullname: Luo, Zhong-Wei
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  givenname: Fu-Xing-Zi
  surname: Li
  fullname: Li, Fu-Xing-Zi
  organization: The Second Xiangya Hospital, Central South University
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  givenname: Jia
  orcidid: 0000-0002-9508-1397
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  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  givenname: Jiang-Shan
  surname: Gong
  fullname: Gong, Jiang-Shan
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  surname: Zou
  fullname: Zou, Jing-Tao
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
– sequence: 11
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  surname: Wang
  fullname: Wang, Qiang
  organization: Department of Laboratory Medicine, Affiliated Zhejiang Hospital, Zhejiang University School of Medicine, Hangzhou
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  surname: Tan
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  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  organization: Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  surname: Wang
  fullname: Wang, Xiao-Kai
  organization: Department of Emergency Medicine, Xiangya Hospital, Central South University
– sequence: 18
  givenname: Ze-Hui
  surname: He
  fullname: He, Ze-Hui
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  surname: Ren
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  organization: The Second Xiangya Hospital, Central South University
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  surname: Liu
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  organization: Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Department of Sports Medicine, Xiangya Hospital, Central South University, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Hunan Key Laboratory of Organ Injury, Aging and Regenerative Medicine, Hunan Key Laboratory of Bone Joint Degeneration and Injury
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  givenname: Ling-Qing
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  organization: The Second Xiangya Hospital, Central South University
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  fullname: Xu, Ran
  organization: The Second Xiangya Hospital, Central South University
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  givenname: Chun-Yuan
  orcidid: 0000-0001-7808-533X
  surname: Chen
  fullname: Chen, Chun-Yuan
  email: chency19@csu.edu.cn
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University
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  givenname: Hui
  orcidid: 0000-0002-8526-2637
  surname: Xie
  fullname: Xie, Hui
  email: huixie@csu.edu.cn
  organization: Department of Orthopedics, Xiangya Hospital, Central South University, Movement System Injury and Repair Research Center, Xiangya Hospital, Central South University, Department of Sports Medicine, Xiangya Hospital, Central South University, National Clinical Research Center for Geriatric Disorders, Xiangya Hospital, Central South University, Hunan Key Laboratory of Organ Injury, Aging and Regenerative Medicine, Hunan Key Laboratory of Bone Joint Degeneration and Injury
BackLink https://www.ncbi.nlm.nih.gov/pubmed/35304471$$D View this record in MEDLINE/PubMed
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Snippet Adipocyte differentiation of bone marrow mesenchymal stem/stromal cells (BMSCs) instead of osteoblast formation contributes to age- and menopause-related...
This study uncovers the role of extracellular vesicles from bone matrix as a messenger in the development of osteoporosis and vascular calcification...
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Adipogenesis
Adipose tissue
Aging
Alendronic acid
Animals
Biomedical materials
Bisphosphonates
Bone marrow
Bone Matrix
Bone resorption
Calcification
Calcification (ectopic)
Cell Differentiation
Extracellular Vesicles
Female
Humanities and Social Sciences
Intravenous administration
Matrix vesicles
Menopause
Mesenchymal Stem Cells
Mesenchyme
Mice
MicroRNAs - genetics
multidisciplinary
Muscles
Oophorectomy
Osteoblastogenesis
Osteogenesis
Osteoporosis
Ovariectomy
Paradoxes
Science
Science (multidisciplinary)
Smooth muscle
Stromal cells
Vesicles
Vitamin D3
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Title Aged bone matrix-derived extracellular vesicles as a messenger for calcification paradox
URI https://link.springer.com/article/10.1038/s41467-022-29191-x
https://www.ncbi.nlm.nih.gov/pubmed/35304471
https://www.proquest.com/docview/2640574031
https://www.proquest.com/docview/2640996965
https://pubmed.ncbi.nlm.nih.gov/PMC8933454
https://doaj.org/article/ab6085afb96c4c6ca3fad64ef9bffdb0
Volume 13
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