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ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway

Cutaneous wound is a soft tissue injury that is difficult to heal during aging. It has been demonstrated that adipose-derived stem cells (ADSCs) and its secreted exosomes exert crucial functions in cutaneous wound healing. The present study aimed to elucidate the mechanism of exosomes derived from A...

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Autores principales: He, Lin, Zhu, Chan, Jia, Jing, Hao, Xiao-Yan, Yu, Xue-Yuan, Liu, Xiang-Yu, Shu, Mao-Guo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2020
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214401/
https://www.ncbi.nlm.nih.gov/pubmed/32342982
http://dx.doi.org/10.1042/BSR20192549
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author He, Lin
Zhu, Chan
Jia, Jing
Hao, Xiao-Yan
Yu, Xue-Yuan
Liu, Xiang-Yu
Shu, Mao-Guo
author_facet He, Lin
Zhu, Chan
Jia, Jing
Hao, Xiao-Yan
Yu, Xue-Yuan
Liu, Xiang-Yu
Shu, Mao-Guo
author_sort He, Lin
collection PubMed
description Cutaneous wound is a soft tissue injury that is difficult to heal during aging. It has been demonstrated that adipose-derived stem cells (ADSCs) and its secreted exosomes exert crucial functions in cutaneous wound healing. The present study aimed to elucidate the mechanism of exosomes derived from ADSCs (ADSC-Exos) containing MALAT1 in wound healing. ADSCs were isolated from human normal subcutaneous adipose tissues and identified by flow cytometry analysis. Exosomes were extracted from ADSC supernatants and MALAT1 expression was determined using qRT-PCR analysis. HaCaT and HDF cells were exposed to hydrogen peroxide (H(2)O(2)) for simulating the skin lesion model. Subsequently, CCK-8, flow cytometry, wound healing and transwell assays were employed to validate the role of ADSC-Exos containing MALAT1 in the skin lesion model. Besides, cells were transfected with sh-MALAT1 to verify the protective role of MALAT1 in wound healing. The binding relationship between MALAT1 and miR-124 were measured by dual-luciferase reporter assay. ADSC-Exos promoted cell proliferation, migration, and inhibited cell apoptosis of HaCaT and HDF cells impaired by H(2)O(2). However, the depletion of MALAT1 in ADSC-Exos lose these protective effects on HaCaT and HDF cells. Moreover, miR-124 was identified to be a target of MALAT1. Furthermore, ADSC-Exos containing MALAT1 could mediate H(2)O(2)-induced wound healing by targeting miR-124 and activating Wnt/β-catenin pathway. ADSC-Exos containing MALAT1 play a positive role in cutaneous wound healing possibly via targeting miR-124 through activating the Wnt/β-catenin pathway, which may provide novel insights into the therapeutic target for cutaneous wound healing.
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spelling pubmed-72144012020-05-22 ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway He, Lin Zhu, Chan Jia, Jing Hao, Xiao-Yan Yu, Xue-Yuan Liu, Xiang-Yu Shu, Mao-Guo Biosci Rep Cell Cycle, Growth & Proliferation Cutaneous wound is a soft tissue injury that is difficult to heal during aging. It has been demonstrated that adipose-derived stem cells (ADSCs) and its secreted exosomes exert crucial functions in cutaneous wound healing. The present study aimed to elucidate the mechanism of exosomes derived from ADSCs (ADSC-Exos) containing MALAT1 in wound healing. ADSCs were isolated from human normal subcutaneous adipose tissues and identified by flow cytometry analysis. Exosomes were extracted from ADSC supernatants and MALAT1 expression was determined using qRT-PCR analysis. HaCaT and HDF cells were exposed to hydrogen peroxide (H(2)O(2)) for simulating the skin lesion model. Subsequently, CCK-8, flow cytometry, wound healing and transwell assays were employed to validate the role of ADSC-Exos containing MALAT1 in the skin lesion model. Besides, cells were transfected with sh-MALAT1 to verify the protective role of MALAT1 in wound healing. The binding relationship between MALAT1 and miR-124 were measured by dual-luciferase reporter assay. ADSC-Exos promoted cell proliferation, migration, and inhibited cell apoptosis of HaCaT and HDF cells impaired by H(2)O(2). However, the depletion of MALAT1 in ADSC-Exos lose these protective effects on HaCaT and HDF cells. Moreover, miR-124 was identified to be a target of MALAT1. Furthermore, ADSC-Exos containing MALAT1 could mediate H(2)O(2)-induced wound healing by targeting miR-124 and activating Wnt/β-catenin pathway. ADSC-Exos containing MALAT1 play a positive role in cutaneous wound healing possibly via targeting miR-124 through activating the Wnt/β-catenin pathway, which may provide novel insights into the therapeutic target for cutaneous wound healing. Portland Press Ltd. 2020-05-11 /pmc/articles/PMC7214401/ /pubmed/32342982 http://dx.doi.org/10.1042/BSR20192549 Text en © 2020 The Author(s). https://creativecommons.org/licenses/by/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY).
spellingShingle Cell Cycle, Growth & Proliferation
He, Lin
Zhu, Chan
Jia, Jing
Hao, Xiao-Yan
Yu, Xue-Yuan
Liu, Xiang-Yu
Shu, Mao-Guo
ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title_full ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title_fullStr ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title_full_unstemmed ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title_short ADSC-Exos containing MALAT1 promotes wound healing by targeting miR-124 through activating Wnt/β-catenin pathway
title_sort adsc-exos containing malat1 promotes wound healing by targeting mir-124 through activating wnt/β-catenin pathway
topic Cell Cycle, Growth & Proliferation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7214401/
https://www.ncbi.nlm.nih.gov/pubmed/32342982
http://dx.doi.org/10.1042/BSR20192549
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