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

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

  • Mol Biol Rep. 2022 Aug;49(8):7337-7345. doi: 10.1007/s11033-022-07524-9.
Yan Wang 1,  Jiaxin Liu 1,  Baocong Yu 2,  Yiran Jin 1,  Jiahui Li 1,  Xiaona Ma 1,  Jianqiang Yu 3,  Jianguo Niu 4,  Xueyun Liang 5
Affiliations

Affiliations

  • 1 Key Laboratory of Ningxia Stem Cell and Regenerative Medicine, General Hospital of Ningxia Medical University, 750001, Yinchuan, China.
  • 2 Ningxia Key Laboratory of Cerebrocranial Diseases, Ningxia Medical University, 750004, Yinchuan, China.
  • 3 School of Pharmacology, Ningxia Medical University, 750004, Yinchuan, China. [email protected].
  • 4 Ningxia Key Laboratory of Cerebrocranial Diseases, Ningxia Medical University, 750004, Yinchuan, China. [email protected].
  • 5 Key Laboratory of Ningxia Stem Cell and Regenerative Medicine, General Hospital of Ningxia Medical University, 750001, Yinchuan, China. [email protected].
PMID: 35585377 DOI: 10.1007/s11033-022-07524-9
Abstract

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.

Keywords

Conditioned medium; MAPK; Mesenchymal stem cells; Neuronal apoptosis; TRPM2.

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