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Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair

Crosstalk between nerves and bone is essential for bone repair, for which Schwann cells (SCs) are crucial in the regulation of the microenvironment. Considering that exosomes are critical paracrine mediators for intercellular communication that exert important effects in tissue repair, the aim of th...

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Detalles Bibliográficos
Autores principales: Wang, Tianchang, Li, Wentao, Zhang, Yuxin, Xu, Xiang, Qiang, Lei, Miao, Weiqiang, Yue, Xiaokun, Jiao, Xin, Zhou, Xianhao, Ma, Zhenjiang, Li, Shuai, Ding, Muliang, Zhu, Junfeng, Yang, Chi, Wang, Hui, Li, Tao, Sun, Xin, Wang, Jinwu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: KeAi Publishing 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10131128/
https://www.ncbi.nlm.nih.gov/pubmed/37122897
http://dx.doi.org/10.1016/j.bioactmat.2023.02.013
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author Wang, Tianchang
Li, Wentao
Zhang, Yuxin
Xu, Xiang
Qiang, Lei
Miao, Weiqiang
Yue, Xiaokun
Jiao, Xin
Zhou, Xianhao
Ma, Zhenjiang
Li, Shuai
Ding, Muliang
Zhu, Junfeng
Yang, Chi
Wang, Hui
Li, Tao
Sun, Xin
Wang, Jinwu
author_facet Wang, Tianchang
Li, Wentao
Zhang, Yuxin
Xu, Xiang
Qiang, Lei
Miao, Weiqiang
Yue, Xiaokun
Jiao, Xin
Zhou, Xianhao
Ma, Zhenjiang
Li, Shuai
Ding, Muliang
Zhu, Junfeng
Yang, Chi
Wang, Hui
Li, Tao
Sun, Xin
Wang, Jinwu
author_sort Wang, Tianchang
collection PubMed
description Crosstalk between nerves and bone is essential for bone repair, for which Schwann cells (SCs) are crucial in the regulation of the microenvironment. Considering that exosomes are critical paracrine mediators for intercellular communication that exert important effects in tissue repair, the aim of this study is to confirm the function and molecular mechanisms of Schwann cell-derived exosomes (SC-exos) on bone regeneration and to propose engineered constructs that simulate SC-mediated nerve–bone crosstalk. SCs promoted the proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs) through exosomes. Subsequent molecular mechanism studies demonstrated that SC-exos promoted BMSC osteogenesis by regulating the TGF-β signaling pathway via let-7c-5p. Interestingly, SC-exos promoted the migration and tube formation performance of endothelial progenitor cells. Furthermore, the SC-exos@G/S constructs were developed by bioprinting technology that simulated SC-mediated nerve–bone crosstalk and improved the bone regeneration microenvironment by releasing SC-exos, exerting the regulatory effect of SCs in the microenvironment to promote innervation, vascularization, and osteogenesis and thus effectively improving bone repair in a cranial defect model. This study demonstrates the important role and underlying mechanism of SCs in regulating bone regeneration through SC-exos and provides a new engineered strategy for bone repair.
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spelling pubmed-101311282023-04-27 Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair Wang, Tianchang Li, Wentao Zhang, Yuxin Xu, Xiang Qiang, Lei Miao, Weiqiang Yue, Xiaokun Jiao, Xin Zhou, Xianhao Ma, Zhenjiang Li, Shuai Ding, Muliang Zhu, Junfeng Yang, Chi Wang, Hui Li, Tao Sun, Xin Wang, Jinwu Bioact Mater Article Crosstalk between nerves and bone is essential for bone repair, for which Schwann cells (SCs) are crucial in the regulation of the microenvironment. Considering that exosomes are critical paracrine mediators for intercellular communication that exert important effects in tissue repair, the aim of this study is to confirm the function and molecular mechanisms of Schwann cell-derived exosomes (SC-exos) on bone regeneration and to propose engineered constructs that simulate SC-mediated nerve–bone crosstalk. SCs promoted the proliferation and differentiation of bone marrow mesenchymal stem cells (BMSCs) through exosomes. Subsequent molecular mechanism studies demonstrated that SC-exos promoted BMSC osteogenesis by regulating the TGF-β signaling pathway via let-7c-5p. Interestingly, SC-exos promoted the migration and tube formation performance of endothelial progenitor cells. Furthermore, the SC-exos@G/S constructs were developed by bioprinting technology that simulated SC-mediated nerve–bone crosstalk and improved the bone regeneration microenvironment by releasing SC-exos, exerting the regulatory effect of SCs in the microenvironment to promote innervation, vascularization, and osteogenesis and thus effectively improving bone repair in a cranial defect model. This study demonstrates the important role and underlying mechanism of SCs in regulating bone regeneration through SC-exos and provides a new engineered strategy for bone repair. KeAi Publishing 2023-04-21 /pmc/articles/PMC10131128/ /pubmed/37122897 http://dx.doi.org/10.1016/j.bioactmat.2023.02.013 Text en © 2023 The Authors https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the CC BY-NC-ND license (http://creativecommons.org/licenses/by-nc-nd/4.0/).
spellingShingle Article
Wang, Tianchang
Li, Wentao
Zhang, Yuxin
Xu, Xiang
Qiang, Lei
Miao, Weiqiang
Yue, Xiaokun
Jiao, Xin
Zhou, Xianhao
Ma, Zhenjiang
Li, Shuai
Ding, Muliang
Zhu, Junfeng
Yang, Chi
Wang, Hui
Li, Tao
Sun, Xin
Wang, Jinwu
Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title_full Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title_fullStr Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title_full_unstemmed Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title_short Bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
title_sort bioprinted constructs that simulate nerve–bone crosstalk to improve microenvironment for bone repair
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10131128/
https://www.ncbi.nlm.nih.gov/pubmed/37122897
http://dx.doi.org/10.1016/j.bioactmat.2023.02.013
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