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Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway

BACKGROUND: The mechanism by which MSC-CM protects neuronal cells against ischemic injury remains to be elucidated. In this study, we aimed to clarify the protective effect of umbilical cord-derived mesenchymal stem cell conditioned medium (UC-MSC-CM) on neuronal oxidative injury and its potential m...

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Autores principales: Wang, Yan, Liu, Jiaxin, Yu, Baocong, Jin, Yiran, Li, Jiahui, Ma, Xiaona, Yu, Jianqiang, Niu, Jianguo, Liang, Xueyun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Springer Netherlands 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9304044/
https://www.ncbi.nlm.nih.gov/pubmed/35585377
http://dx.doi.org/10.1007/s11033-022-07524-9
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author Wang, Yan
Liu, Jiaxin
Yu, Baocong
Jin, Yiran
Li, Jiahui
Ma, Xiaona
Yu, Jianqiang
Niu, Jianguo
Liang, Xueyun
author_facet Wang, Yan
Liu, Jiaxin
Yu, Baocong
Jin, Yiran
Li, Jiahui
Ma, Xiaona
Yu, Jianqiang
Niu, Jianguo
Liang, Xueyun
author_sort Wang, Yan
collection PubMed
description BACKGROUND: The mechanism by which MSC-CM protects neuronal cells against ischemic injury remains to be elucidated. In this study, we aimed to clarify the protective effect of umbilical cord-derived mesenchymal stem cell conditioned medium (UC-MSC-CM) on neuronal oxidative injury and its potential mechanism. METHODS AND RESULTS: Neuronal oxidative damage was mimicked by H2O2 treatment of the HT22 cell line. The numbers of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Furthermore, SOD protein expression was increased in the MSC-CM group compared with that in the H2O2 group. The H2O2-induced TRPM2-like currents in HT22 cells were attenuated by MSC-CM treatment. In addition, H2O2 treatment downregulated the expression of p-JNK protein in HT22 cells, and this the downward trend was reversed by incubation with MSC-CM. CONCLUSIONS: UC-MSC-CM protects neurons against oxidative injury, possibly by inhibiting activation of TRPM2 and the JNK signaling pathway.
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spelling pubmed-93040442022-07-23 Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway Wang, Yan Liu, Jiaxin Yu, Baocong Jin, Yiran Li, Jiahui Ma, Xiaona Yu, Jianqiang Niu, Jianguo Liang, Xueyun Mol Biol Rep Original Article BACKGROUND: The mechanism by which MSC-CM protects neuronal cells against ischemic injury remains to be elucidated. In this study, we aimed to clarify the protective effect of umbilical cord-derived mesenchymal stem cell conditioned medium (UC-MSC-CM) on neuronal oxidative injury and its potential mechanism. METHODS AND RESULTS: Neuronal oxidative damage was mimicked by H2O2 treatment of the HT22 cell line. The numbers of cleaved-Caspase-3-positive cells and protein expression of Caspase-9 induced by H2O2 treatment were decreased by UC-MSC-CM treatment. Furthermore, SOD protein expression was increased in the MSC-CM group compared with that in the H2O2 group. The H2O2-induced TRPM2-like currents in HT22 cells were attenuated by MSC-CM treatment. In addition, H2O2 treatment downregulated the expression of p-JNK protein in HT22 cells, and this the downward trend was reversed by incubation with MSC-CM. CONCLUSIONS: UC-MSC-CM protects neurons against oxidative injury, possibly by inhibiting activation of TRPM2 and the JNK signaling pathway. Springer Netherlands 2022-05-18 2022 /pmc/articles/PMC9304044/ /pubmed/35585377 http://dx.doi.org/10.1007/s11033-022-07524-9 Text en © The Author(s) 2022 https://creativecommons.org/licenses/by/4.0/Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) .
spellingShingle Original Article
Wang, Yan
Liu, Jiaxin
Yu, Baocong
Jin, Yiran
Li, Jiahui
Ma, Xiaona
Yu, Jianqiang
Niu, Jianguo
Liang, Xueyun
Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title_full Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title_fullStr Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title_full_unstemmed Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title_short Umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of TRPM2 activation and the JNK signaling pathway
title_sort umbilical cord-derived mesenchymal stem cell conditioned medium reverses neuronal oxidative injury by inhibition of trpm2 activation and the jnk signaling pathway
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9304044/
https://www.ncbi.nlm.nih.gov/pubmed/35585377
http://dx.doi.org/10.1007/s11033-022-07524-9
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