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Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis

BACKGROUND: Postmenopausal osteoporosis (PMO) that results from estrogen withdrawal is the most common primary osteoporosis among older women. However, little is known about the mechanism of PMO, and effective treatment of PMO is limited. METHODS: We used real-time polymerase chain reaction (qPCR),...

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Autores principales: Li, Lu, Zhou, Xin, Zhang, Jun-tao, Liu, Ai-feng, Zhang, Chao, Han, Jin-chang, Zhang, Xiao-qing, Wu, Si, Zhang, Xiao-yu, Lv, Fu-quan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791800/
https://www.ncbi.nlm.nih.gov/pubmed/33413543
http://dx.doi.org/10.1186/s13018-020-02160-0
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author Li, Lu
Zhou, Xin
Zhang, Jun-tao
Liu, Ai-feng
Zhang, Chao
Han, Jin-chang
Zhang, Xiao-qing
Wu, Si
Zhang, Xiao-yu
Lv, Fu-quan
author_facet Li, Lu
Zhou, Xin
Zhang, Jun-tao
Liu, Ai-feng
Zhang, Chao
Han, Jin-chang
Zhang, Xiao-qing
Wu, Si
Zhang, Xiao-yu
Lv, Fu-quan
author_sort Li, Lu
collection PubMed
description BACKGROUND: Postmenopausal osteoporosis (PMO) that results from estrogen withdrawal is the most common primary osteoporosis among older women. However, little is known about the mechanism of PMO, and effective treatment of PMO is limited. METHODS: We used real-time polymerase chain reaction (qPCR), Western blotting, and RNA pull down to investigate the relationship between miR-186 and MOB Kinase Activator 1A (Mob1). Also, we investigated the effect of exosome in osteogenesis using alkaline phosphatase (ALP) staining. And hematoxylin eosin (HE) staining was used to verify the osteogenesis in PMO model. RESULTS: Exosomal miR-186 plays an important role in bone formation. The results of miRNA-seq and q-PCR showed that miR-186 was upregulated in a PMO + Exo treatment group. Results of RNA-pull down and luciferase reporter assays verified interactions between miR-186 and Mob1. We also verified the Hippo signaling pathway plays an important role in osteogenesis. CONCLUSIONS: We concluded that exosomes derived from human bone marrow mesenchymal stem cells (hBMSCs) can transfer miR-186 to promote osteogenesis in ovariectomy (OVX) rats through the Hippo signaling pathway.
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spelling pubmed-77918002021-01-11 Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis Li, Lu Zhou, Xin Zhang, Jun-tao Liu, Ai-feng Zhang, Chao Han, Jin-chang Zhang, Xiao-qing Wu, Si Zhang, Xiao-yu Lv, Fu-quan J Orthop Surg Res Research Article BACKGROUND: Postmenopausal osteoporosis (PMO) that results from estrogen withdrawal is the most common primary osteoporosis among older women. However, little is known about the mechanism of PMO, and effective treatment of PMO is limited. METHODS: We used real-time polymerase chain reaction (qPCR), Western blotting, and RNA pull down to investigate the relationship between miR-186 and MOB Kinase Activator 1A (Mob1). Also, we investigated the effect of exosome in osteogenesis using alkaline phosphatase (ALP) staining. And hematoxylin eosin (HE) staining was used to verify the osteogenesis in PMO model. RESULTS: Exosomal miR-186 plays an important role in bone formation. The results of miRNA-seq and q-PCR showed that miR-186 was upregulated in a PMO + Exo treatment group. Results of RNA-pull down and luciferase reporter assays verified interactions between miR-186 and Mob1. We also verified the Hippo signaling pathway plays an important role in osteogenesis. CONCLUSIONS: We concluded that exosomes derived from human bone marrow mesenchymal stem cells (hBMSCs) can transfer miR-186 to promote osteogenesis in ovariectomy (OVX) rats through the Hippo signaling pathway. BioMed Central 2021-01-07 /pmc/articles/PMC7791800/ /pubmed/33413543 http://dx.doi.org/10.1186/s13018-020-02160-0 Text en © The Author(s) 2021 Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.
spellingShingle Research Article
Li, Lu
Zhou, Xin
Zhang, Jun-tao
Liu, Ai-feng
Zhang, Chao
Han, Jin-chang
Zhang, Xiao-qing
Wu, Si
Zhang, Xiao-yu
Lv, Fu-quan
Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title_full Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title_fullStr Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title_full_unstemmed Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title_short Exosomal miR-186 derived from BMSCs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
title_sort exosomal mir-186 derived from bmscs promote osteogenesis through hippo signaling pathway in postmenopausal osteoporosis
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7791800/
https://www.ncbi.nlm.nih.gov/pubmed/33413543
http://dx.doi.org/10.1186/s13018-020-02160-0
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