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Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway

microRNA‐126 (miR‐126), an endothelial‐specific miRNA, is associated with vascular homeostasis and angiogenesis. However, the efficiency of miR‐126‐based treatment is partially compromised due to the low efficiency of miRNA delivery in vivo. Lately, exosomes have emerged as a natural tool for therap...

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Autores principales: Zhang, Lei, Ouyang, Pengrong, He, Gaole, Wang, Xiaowei, Song, Defu, Yang, Yijun, He, Xijing
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/PMC7882955/
https://www.ncbi.nlm.nih.gov/pubmed/33350092
http://dx.doi.org/10.1111/jcmm.16192
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author Zhang, Lei
Ouyang, Pengrong
He, Gaole
Wang, Xiaowei
Song, Defu
Yang, Yijun
He, Xijing
author_facet Zhang, Lei
Ouyang, Pengrong
He, Gaole
Wang, Xiaowei
Song, Defu
Yang, Yijun
He, Xijing
author_sort Zhang, Lei
collection PubMed
description microRNA‐126 (miR‐126), an endothelial‐specific miRNA, is associated with vascular homeostasis and angiogenesis. However, the efficiency of miR‐126‐based treatment is partially compromised due to the low efficiency of miRNA delivery in vivo. Lately, exosomes have emerged as a natural tool for therapeutic molecule delivery. Herein, we investigated whether exosomes derived from bone marrow mesenchymal stem cells (BMMSCs) can be utilized to deliver miR‐126 to promote angiogenesis. Exosomes were isolated from BMMSCs overexpressed with miR‐126 (Exo‐miR‐126) by ultracentrifugation. In vitro study, Exo‐miR‐126 treatment promoted the proliferation, migration and angiogenesis of human umbilical vein endothelial cells (HUVECs). Furthermore, the gene/protein expression of angiogenesis‐related vascular endothelial growth factor (VEGF) and angiotensin‐1 (Ang‐1) were up‐regulated after incubation with Exo‐miR‐126. Additionally, the expression level of phosphoinositol‐3 kinase regulatory subunit 2 (PIK3R2) showed an inverse correlation with miR‐126 in HUVECs. Particularly, the Exo‐miR‐126 treatment contributed to enhanced angiogenesis of HUVECs by targeting PIK3R2 to activate the PI3K/Akt signalling pathway. Similarly, Exo‐miR‐126 administration profoundly increased the number of newly formed capillaries in wound sites and accelerated the wound healing in vivo. The results demonstrate that exosomes derived from BMMSCs combined with miR‐126 may be a promising strategy to promote angiogenesis.
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spelling pubmed-78829552021-02-19 Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway Zhang, Lei Ouyang, Pengrong He, Gaole Wang, Xiaowei Song, Defu Yang, Yijun He, Xijing J Cell Mol Med Original Articles microRNA‐126 (miR‐126), an endothelial‐specific miRNA, is associated with vascular homeostasis and angiogenesis. However, the efficiency of miR‐126‐based treatment is partially compromised due to the low efficiency of miRNA delivery in vivo. Lately, exosomes have emerged as a natural tool for therapeutic molecule delivery. Herein, we investigated whether exosomes derived from bone marrow mesenchymal stem cells (BMMSCs) can be utilized to deliver miR‐126 to promote angiogenesis. Exosomes were isolated from BMMSCs overexpressed with miR‐126 (Exo‐miR‐126) by ultracentrifugation. In vitro study, Exo‐miR‐126 treatment promoted the proliferation, migration and angiogenesis of human umbilical vein endothelial cells (HUVECs). Furthermore, the gene/protein expression of angiogenesis‐related vascular endothelial growth factor (VEGF) and angiotensin‐1 (Ang‐1) were up‐regulated after incubation with Exo‐miR‐126. Additionally, the expression level of phosphoinositol‐3 kinase regulatory subunit 2 (PIK3R2) showed an inverse correlation with miR‐126 in HUVECs. Particularly, the Exo‐miR‐126 treatment contributed to enhanced angiogenesis of HUVECs by targeting PIK3R2 to activate the PI3K/Akt signalling pathway. Similarly, Exo‐miR‐126 administration profoundly increased the number of newly formed capillaries in wound sites and accelerated the wound healing in vivo. The results demonstrate that exosomes derived from BMMSCs combined with miR‐126 may be a promising strategy to promote angiogenesis. John Wiley and Sons Inc. 2020-12-21 2021-02 /pmc/articles/PMC7882955/ /pubmed/33350092 http://dx.doi.org/10.1111/jcmm.16192 Text en © 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and 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
Zhang, Lei
Ouyang, Pengrong
He, Gaole
Wang, Xiaowei
Song, Defu
Yang, Yijun
He, Xijing
Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title_full Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title_fullStr Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title_full_unstemmed Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title_short Exosomes from microRNA‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the PIK3R2‐mediated PI3K/Akt signalling pathway
title_sort exosomes from microrna‐126 overexpressing mesenchymal stem cells promote angiogenesis by targeting the pik3r2‐mediated pi3k/akt signalling pathway
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7882955/
https://www.ncbi.nlm.nih.gov/pubmed/33350092
http://dx.doi.org/10.1111/jcmm.16192
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