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Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis

OBJECTIVES: It is of profound significance for clinical bone regeneration to clarify the specific molecular mechanism from which we found that osteogenic differentiation of adipose‐derived stem cells (ADSCs) will be probably promoted by exosomes. MATERIALS AND METHODS: By means of lentiviral transfe...

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Detalles Bibliográficos
Autores principales: Yang, Shude, Guo, Shu, Tong, Shuang, Sun, Xu
Formato: Online Artículo Texto
Lenguaje:English
Publicado: John Wiley and Sons Inc. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574877/
https://www.ncbi.nlm.nih.gov/pubmed/32808361
http://dx.doi.org/10.1111/cpr.12890
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author Yang, Shude
Guo, Shu
Tong, Shuang
Sun, Xu
author_facet Yang, Shude
Guo, Shu
Tong, Shuang
Sun, Xu
author_sort Yang, Shude
collection PubMed
description OBJECTIVES: It is of profound significance for clinical bone regeneration to clarify the specific molecular mechanism from which we found that osteogenic differentiation of adipose‐derived stem cells (ADSCs) will be probably promoted by exosomes. MATERIALS AND METHODS: By means of lentiviral transfection, miR‐130a‐3p overexpression and knockdown ADSCs were constructed. Alizarin Red S was used to detect the calcium deposits, and qPCR was used to detect osteogenesis‐related genes, to verify the effect of miR‐130a‐3p on the osteogenic differentiation of ADSCs. CCK‐8 was used to detect the effect of miR‐130a‐3p on the proliferation of ADSCs. The target binding between miR‐130a‐3p and SIRT7 was verified by dual‐luciferase reporter gene assay. Furthermore, the role of Wnt signalling pathway in the regulation of ADSCs osteogenesis and differentiation by miR‐130a‐3p was further verified by detecting osteogenic‐related genes and proteins and alkaline phosphatase activity. RESULTS: (a) Overexpression of miR‐130a‐3p can enhance the osteogenic differentiation of ADSCs while reducing protein and mRNA levels of SIRT7, a target of miR‐130a‐3p. (b) Our study further found that overexpression of miR‐130a‐3p leads to down‐regulation of SIRT7 expression with up‐regulation of Wnt signalling pathway‐associated protein. (c) Overexpression of miR‐130a‐3p inhibited proliferation of ADSCs, while knockdown promoted it. CONCLUSIONS: The obtained findings indicate that exosomal miR‐130a‐3p can promote osteogenic differentiation of ADSCs partly by mediating SIRT7/Wnt/β‐catenin axis, which will hence promote the application of exosomal microRNA in the field of bone regeneration.
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spelling pubmed-75748772020-10-23 Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis Yang, Shude Guo, Shu Tong, Shuang Sun, Xu Cell Prolif Original Articles OBJECTIVES: It is of profound significance for clinical bone regeneration to clarify the specific molecular mechanism from which we found that osteogenic differentiation of adipose‐derived stem cells (ADSCs) will be probably promoted by exosomes. MATERIALS AND METHODS: By means of lentiviral transfection, miR‐130a‐3p overexpression and knockdown ADSCs were constructed. Alizarin Red S was used to detect the calcium deposits, and qPCR was used to detect osteogenesis‐related genes, to verify the effect of miR‐130a‐3p on the osteogenic differentiation of ADSCs. CCK‐8 was used to detect the effect of miR‐130a‐3p on the proliferation of ADSCs. The target binding between miR‐130a‐3p and SIRT7 was verified by dual‐luciferase reporter gene assay. Furthermore, the role of Wnt signalling pathway in the regulation of ADSCs osteogenesis and differentiation by miR‐130a‐3p was further verified by detecting osteogenic‐related genes and proteins and alkaline phosphatase activity. RESULTS: (a) Overexpression of miR‐130a‐3p can enhance the osteogenic differentiation of ADSCs while reducing protein and mRNA levels of SIRT7, a target of miR‐130a‐3p. (b) Our study further found that overexpression of miR‐130a‐3p leads to down‐regulation of SIRT7 expression with up‐regulation of Wnt signalling pathway‐associated protein. (c) Overexpression of miR‐130a‐3p inhibited proliferation of ADSCs, while knockdown promoted it. CONCLUSIONS: The obtained findings indicate that exosomal miR‐130a‐3p can promote osteogenic differentiation of ADSCs partly by mediating SIRT7/Wnt/β‐catenin axis, which will hence promote the application of exosomal microRNA in the field of bone regeneration. John Wiley and Sons Inc. 2020-08-17 /pmc/articles/PMC7574877/ /pubmed/32808361 http://dx.doi.org/10.1111/cpr.12890 Text en © 2020 The Authors. Cell Proliferation published by John Wiley & Sons Ltd This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
spellingShingle Original Articles
Yang, Shude
Guo, Shu
Tong, Shuang
Sun, Xu
Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title_full Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title_fullStr Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title_full_unstemmed Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title_short Exosomal miR‐130a‐3p regulates osteogenic differentiation of Human Adipose‐Derived stem cells through mediating SIRT7/Wnt/β‐catenin axis
title_sort exosomal mir‐130a‐3p regulates osteogenic differentiation of human adipose‐derived stem cells through mediating sirt7/wnt/β‐catenin axis
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7574877/
https://www.ncbi.nlm.nih.gov/pubmed/32808361
http://dx.doi.org/10.1111/cpr.12890
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