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PARK7 enhances antioxidative-stress processes of BMSCs via the ERK1/2 pathway.
Journal of Cellular Biochemistry ( IF 3.0 ) Pub Date : 2020-09-12 , DOI: 10.1002/jcb.29845 Fei Zhang 1, 2 , Wuxun Peng 1, 2 , Jian Zhang 1, 2 , Lei Wang 3 , Wentao Dong 1, 2 , Yinggang Zheng 4 , Zhenwen Wang 5 , Zhihong Xie 2 , Tao Wang 2 , Chuan Wang 2 , Yanglin Yan 2
Journal of Cellular Biochemistry ( IF 3.0 ) Pub Date : 2020-09-12 , DOI: 10.1002/jcb.29845 Fei Zhang 1, 2 , Wuxun Peng 1, 2 , Jian Zhang 1, 2 , Lei Wang 3 , Wentao Dong 1, 2 , Yinggang Zheng 4 , Zhenwen Wang 5 , Zhihong Xie 2 , Tao Wang 2 , Chuan Wang 2 , Yanglin Yan 2
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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 H2O2 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 H2O2 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.
中文翻译：
PARK7 通过 ERK1/2 通路增强 BMSCs 的抗氧化应激过程。
病变周围微环境中的氧化应激诱导移植的骨髓间充质干细胞（BMSCs）凋亡。因此，迫切需要改善移植骨髓间充质干细胞的抗氧化应激过程以进一步促进其存活。本研究报告了帕金森病蛋白 7 (PARK7) 在增强 BMSCs 抗氧化活性中的作用和机制。我们使用 PARK7 慢病毒转染 BMSCs 以上调或下调 PARK7，然后使用 H 2 O 2在体外模拟 BMSCs 的氧化应激。PARK7的过表达有效降低活性氧和丙二醛，保护线粒体膜电位，抵抗氧化应激诱导的BMSCs凋亡，但PARK7的表达下调，这些结果被逆转。同时，我们还发现 PARK7 的过表达增加了细胞外调节蛋白激酶 1/2 (ERK1/2) 磷酸化和核易位，以及上调 Elk1 磷酸化和超氧化物歧化酶 (SOD) 表达。相比之下，当使用U0126阻断ERK1/2通路时，ERK1/2和Elk1磷酸化水平下调，ERK1/2核转位和SOD含量显着降低，PARK7过度表达诱导的抗氧化活性被完全阻断。总的来说，2 O 2通过激活 ERK1/2 信号通路。我们的研究结果可能会指导 PARK7 特异性策略的开发，以提高 BMSCs 的移植功效。
更新日期：2020-09-12
中文翻译：
PARK7 通过 ERK1/2 通路增强 BMSCs 的抗氧化应激过程。
病变周围微环境中的氧化应激诱导移植的骨髓间充质干细胞（BMSCs）凋亡。因此，迫切需要改善移植骨髓间充质干细胞的抗氧化应激过程以进一步促进其存活。本研究报告了帕金森病蛋白 7 (PARK7) 在增强 BMSCs 抗氧化活性中的作用和机制。我们使用 PARK7 慢病毒转染 BMSCs 以上调或下调 PARK7，然后使用 H 2 O 2在体外模拟 BMSCs 的氧化应激。PARK7的过表达有效降低活性氧和丙二醛，保护线粒体膜电位，抵抗氧化应激诱导的BMSCs凋亡，但PARK7的表达下调，这些结果被逆转。同时，我们还发现 PARK7 的过表达增加了细胞外调节蛋白激酶 1/2 (ERK1/2) 磷酸化和核易位，以及上调 Elk1 磷酸化和超氧化物歧化酶 (SOD) 表达。相比之下，当使用U0126阻断ERK1/2通路时，ERK1/2和Elk1磷酸化水平下调，ERK1/2核转位和SOD含量显着降低，PARK7过度表达诱导的抗氧化活性被完全阻断。总的来说，2 O 2通过激活 ERK1/2 信号通路。我们的研究结果可能会指导 PARK7 特异性策略的开发，以提高 BMSCs 的移植功效。
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