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PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway

Oxidative stresss in the microenvironment surrounding lesions induces apoptosis of transplanted bone‐marrow‐derived mesenchymal stem cells (BMSCs). Hence, there is an urgent need for improving antioxidative‐stress processes of transplanted BMSCs to further promote their survival. The present study r...

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Autores principales: Zhang, Fei, Peng, Wuxun, Zhang, Jian, Wang, Lei, Dong, Wentao, Zheng, Yinggang, Wang, Zhenwen, Xie, Zhihong, Wang, Tao, Wang, Chuan, Yan, Yanglin
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/PMC7820948/
https://www.ncbi.nlm.nih.gov/pubmed/32918333
http://dx.doi.org/10.1002/jcb.29845
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author Zhang, Fei
Peng, Wuxun
Zhang, Jian
Wang, Lei
Dong, Wentao
Zheng, Yinggang
Wang, Zhenwen
Xie, Zhihong
Wang, Tao
Wang, Chuan
Yan, Yanglin
author_facet Zhang, Fei
Peng, Wuxun
Zhang, Jian
Wang, Lei
Dong, Wentao
Zheng, Yinggang
Wang, Zhenwen
Xie, Zhihong
Wang, Tao
Wang, Chuan
Yan, Yanglin
author_sort Zhang, Fei
collection PubMed
description Oxidative stresss in the microenvironment surrounding lesions induces apoptosis of transplanted bone‐marrow‐derived mesenchymal stem cells (BMSCs). Hence, there is an urgent need for improving antioxidative‐stress processes of transplanted BMSCs to further promote their survival. The present study reports the role and mechanism of Parkinson's disease protein 7 (PARK7) in enhancing antioxidative activity in BMSCs. We used a PARK7 lentivirus to transfect BMSCs to up‐ or downregulate PARK7, and then used H(2)O(2) to simulate oxidative stress in BMSCs in vitro. Overexpression of PARK7 effectively reduced reactive oxygen species and malondialdehyde, protected mitochondrial membrane potential, and resisted oxidative‐stress‐induced apoptosis of BMSCs, but the expression of PARK7 was downregulated, these results were reversed. At the same time, we also found that overexpression of PARK7 increased extracellular‐regulated protein kinase 1/2 (ERK1/2) phosphorylation and nuclear translocation, as well as upregulated Elk1 phosphorylation and superoxide dismutase (SOD) expression. In contrast, when U0126 was used to block the ERK1/2 pathway, ERK1/2 and Elk1 phosphorylation levels were downregulated, ERK1/2 nuclear translocation and SOD content were significantly reduced, and PARK7‐overexperssion‐induced antioxidative activity was completely blocked. Collectively, our results suggest that PARK7 overexpression increased antioxidative‐stress processes and survival of BMSCs subjected to H(2)O(2) via activating the ERK1/2 signaling pathway. Our findings may guide the development of a PARK7‐specific strategy for improving the transplantation efficacy of BMSCs.
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spelling pubmed-78209482021-01-26 PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway Zhang, Fei Peng, Wuxun Zhang, Jian Wang, Lei Dong, Wentao Zheng, Yinggang Wang, Zhenwen Xie, Zhihong Wang, Tao Wang, Chuan Yan, Yanglin J Cell Biochem Research Articles Oxidative stresss in the microenvironment surrounding lesions induces apoptosis of transplanted bone‐marrow‐derived mesenchymal stem cells (BMSCs). Hence, there is an urgent need for improving antioxidative‐stress processes of transplanted BMSCs to further promote their survival. The present study reports the role and mechanism of Parkinson's disease protein 7 (PARK7) in enhancing antioxidative activity in BMSCs. We used a PARK7 lentivirus to transfect BMSCs to up‐ or downregulate PARK7, and then used H(2)O(2) to simulate oxidative stress in BMSCs in vitro. Overexpression of PARK7 effectively reduced reactive oxygen species and malondialdehyde, protected mitochondrial membrane potential, and resisted oxidative‐stress‐induced apoptosis of BMSCs, but the expression of PARK7 was downregulated, these results were reversed. At the same time, we also found that overexpression of PARK7 increased extracellular‐regulated protein kinase 1/2 (ERK1/2) phosphorylation and nuclear translocation, as well as upregulated Elk1 phosphorylation and superoxide dismutase (SOD) expression. In contrast, when U0126 was used to block the ERK1/2 pathway, ERK1/2 and Elk1 phosphorylation levels were downregulated, ERK1/2 nuclear translocation and SOD content were significantly reduced, and PARK7‐overexperssion‐induced antioxidative activity was completely blocked. Collectively, our results suggest that PARK7 overexpression increased antioxidative‐stress processes and survival of BMSCs subjected to H(2)O(2) via activating the ERK1/2 signaling pathway. Our findings may guide the development of a PARK7‐specific strategy for improving the transplantation efficacy of BMSCs. John Wiley and Sons Inc. 2020-09-12 2021-02 /pmc/articles/PMC7820948/ /pubmed/32918333 http://dx.doi.org/10.1002/jcb.29845 Text en © 2020 The Authors. Journal of Cellular Biochemistry Published by Wiley Periodicals LLC This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.
spellingShingle Research Articles
Zhang, Fei
Peng, Wuxun
Zhang, Jian
Wang, Lei
Dong, Wentao
Zheng, Yinggang
Wang, Zhenwen
Xie, Zhihong
Wang, Tao
Wang, Chuan
Yan, Yanglin
PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title_full PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title_fullStr PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title_full_unstemmed PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title_short PARK7 enhances antioxidative‐stress processes of BMSCs via the ERK1/2 pathway
title_sort park7 enhances antioxidative‐stress processes of bmscs via the erk1/2 pathway
topic Research Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7820948/
https://www.ncbi.nlm.nih.gov/pubmed/32918333
http://dx.doi.org/10.1002/jcb.29845
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