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 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..
Medienart: |
Artikel |
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Erscheinungsjahr: |
2022 |
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Erschienen: |
2022 |
Enthalten in: |
Zur Gesamtaufnahme - volume:49 |
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Enthalten in: |
Molecular biology reports - 49(2022), 8 vom: 18. Mai, Seite 7337-7345 |
Sprache: |
Englisch |
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Beteiligte Personen: |
Wang, Yan [VerfasserIn] |
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Links: |
Volltext [lizenzpflichtig] |
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Themen: |
Conditioned medium |
Anmerkungen: |
© The Author(s) 2022 |
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doi: |
10.1007/s11033-022-07524-9 |
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funding: |
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PPN (Katalog-ID): |
OLC2079201387 |
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520 | |a 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. | ||
650 | 4 | |a Mesenchymal stem cells | |
650 | 4 | |a Conditioned medium | |
650 | 4 | |a TRPM2 | |
650 | 4 | |a Neuronal apoptosis | |
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700 | 1 | |a Liu, Jiaxin |4 aut | |
700 | 1 | |a Yu, Baocong |4 aut | |
700 | 1 | |a Jin, Yiran |4 aut | |
700 | 1 | |a Li, Jiahui |4 aut | |
700 | 1 | |a Ma, Xiaona |4 aut | |
700 | 1 | |a Yu, Jianqiang |4 aut | |
700 | 1 | |a Niu, Jianguo |4 aut | |
700 | 1 | |a Liang, Xueyun |0 (orcid)0000-0002-4735-4418 |4 aut | |
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