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Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways

OBJECTIVE: Adipose‐derived mesenchymal stem cells (ADSCs) offer great promise as cell therapy for ischaemic diseases. Due to their poor survival in the ischaemic environment, the therapeutic efficacy of ADSCs is still relatively low. Interleukin‐11 (IL‐11) has been shown to play a key role in promot...

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Autores principales: Yang, Wenlong, Zhang, Shuning, Ou, Tiantong, Jiang, Hao, Jia, Daile, Qi, Zhiyong, Zou, Yunzeng, Qian, Juying, Sun, Aijun, Ge, Junbo
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/PMC7260062/
https://www.ncbi.nlm.nih.gov/pubmed/32270546
http://dx.doi.org/10.1111/cpr.12771
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author Yang, Wenlong
Zhang, Shuning
Ou, Tiantong
Jiang, Hao
Jia, Daile
Qi, Zhiyong
Zou, Yunzeng
Qian, Juying
Sun, Aijun
Ge, Junbo
author_facet Yang, Wenlong
Zhang, Shuning
Ou, Tiantong
Jiang, Hao
Jia, Daile
Qi, Zhiyong
Zou, Yunzeng
Qian, Juying
Sun, Aijun
Ge, Junbo
author_sort Yang, Wenlong
collection PubMed
description OBJECTIVE: Adipose‐derived mesenchymal stem cells (ADSCs) offer great promise as cell therapy for ischaemic diseases. Due to their poor survival in the ischaemic environment, the therapeutic efficacy of ADSCs is still relatively low. Interleukin‐11 (IL‐11) has been shown to play a key role in promoting cell proliferation and protecting cells from oxidative stress injury. The aim of this study was to determine whether IL‐11 could improve therapeutic efficacy of ADSCs in ischaemic diseases. METHODS AND RESULTS: ADSCs were prepared from inguinal subcutaneous adipose tissue and exposed to hypoxic environment. The protein expression of IL‐11 was decreased after hypoxic treatment. In addition, ADSCs viability was increased after IL‐11 treatment under hypoxia. Moreover, IL‐11 enhanced ADSCs viability in a dose‐dependent manner under normoxia. Importantly, IL‐11 promoted ADSCs proliferation and migration and protected ADSCs against hydrogen peroxide‐induced cellular death. Notably, IL‐11 enhanced ADSCs proliferation and migration, also promoted cell survival and apoptosis resistance by STAT3 signalling. In vivo, mice were subjected to limb ischaemia and treated with IL‐11 overexpression ADSCs and control ADSCs. IL‐11 overexpression ADSCs improved perfusion recovery in the ischaemic muscles. CONCLUSIONS: We provide the evidence that IL‐11 promoted ADSCs proliferation, stimulated ADSCs migration and attenuated ADSCs apoptosis by activation of STAT3 signalling. These results suggest that IL‐11 facilitated ADSCs engraftment in ischaemic tissue, thereby enhanced ADSCs therapeutic efficacy.
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spelling pubmed-72600622020-06-01 Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways Yang, Wenlong Zhang, Shuning Ou, Tiantong Jiang, Hao Jia, Daile Qi, Zhiyong Zou, Yunzeng Qian, Juying Sun, Aijun Ge, Junbo Cell Prolif Original Articles OBJECTIVE: Adipose‐derived mesenchymal stem cells (ADSCs) offer great promise as cell therapy for ischaemic diseases. Due to their poor survival in the ischaemic environment, the therapeutic efficacy of ADSCs is still relatively low. Interleukin‐11 (IL‐11) has been shown to play a key role in promoting cell proliferation and protecting cells from oxidative stress injury. The aim of this study was to determine whether IL‐11 could improve therapeutic efficacy of ADSCs in ischaemic diseases. METHODS AND RESULTS: ADSCs were prepared from inguinal subcutaneous adipose tissue and exposed to hypoxic environment. The protein expression of IL‐11 was decreased after hypoxic treatment. In addition, ADSCs viability was increased after IL‐11 treatment under hypoxia. Moreover, IL‐11 enhanced ADSCs viability in a dose‐dependent manner under normoxia. Importantly, IL‐11 promoted ADSCs proliferation and migration and protected ADSCs against hydrogen peroxide‐induced cellular death. Notably, IL‐11 enhanced ADSCs proliferation and migration, also promoted cell survival and apoptosis resistance by STAT3 signalling. In vivo, mice were subjected to limb ischaemia and treated with IL‐11 overexpression ADSCs and control ADSCs. IL‐11 overexpression ADSCs improved perfusion recovery in the ischaemic muscles. CONCLUSIONS: We provide the evidence that IL‐11 promoted ADSCs proliferation, stimulated ADSCs migration and attenuated ADSCs apoptosis by activation of STAT3 signalling. These results suggest that IL‐11 facilitated ADSCs engraftment in ischaemic tissue, thereby enhanced ADSCs therapeutic efficacy. John Wiley and Sons Inc. 2020-04-09 /pmc/articles/PMC7260062/ /pubmed/32270546 http://dx.doi.org/10.1111/cpr.12771 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, Wenlong
Zhang, Shuning
Ou, Tiantong
Jiang, Hao
Jia, Daile
Qi, Zhiyong
Zou, Yunzeng
Qian, Juying
Sun, Aijun
Ge, Junbo
Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title_full Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title_fullStr Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title_full_unstemmed Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title_short Interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via STAT3 signalling pathways
title_sort interleukin‐11 regulates the fate of adipose‐derived mesenchymal stem cells via stat3 signalling pathways
topic Original Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7260062/
https://www.ncbi.nlm.nih.gov/pubmed/32270546
http://dx.doi.org/10.1111/cpr.12771
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