2. Academic Validation
  3. Mechanism of mild hypothermia induced cold shock protein protecting neural stem cells

Mechanism of mild hypothermia induced cold shock protein protecting neural stem cells

  • Brain Res Bull. 2025 Oct 15:231:111555. doi: 10.1016/j.brainresbull.2025.111555.
Yuanhui Sun 1,  Jingwen Xue 1,  Liangliang Zhang 2,  Zhichao Zhang 3,  Sha Sha 2,  Qi Sun 2,  Lan Gao 2,  Hao Li 4,  Qindong Shi 5
Affiliations

Affiliations

  • 1 Department of Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; The Shaanxi Provincial Key Laboratory of Sepsis in Critical Care Medicine, the First Affiliated Hospital of Xi 'an Jiaotong University, Xi'an, Shaanxi, China.
  • 2 Department of Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China.
  • 3 Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, Shaanxi, China.
  • 4 Department of Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; The Shaanxi Provincial Key Laboratory of Sepsis in Critical Care Medicine, the First Affiliated Hospital of Xi 'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address: [email protected].
  • 5 Department of Critical Care Medicine, The First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, Shaanxi, China; Department of Critical Care Medicine, The Affiliated Tumor Hospital of Xinjiang Medical University, Urumqi, Xinjiang, China; The Shaanxi Provincial Key Laboratory of Sepsis in Critical Care Medicine, the First Affiliated Hospital of Xi 'an Jiaotong University, Xi'an, Shaanxi, China. Electronic address: [email protected].
PMID: 40975409 DOI: 10.1016/j.brainresbull.2025.111555
Abstract

Cardiac arrest (CA) is a leading cause of death in humans. Our previous research confirmed that after CA/cardiopulmonary resuscitation, mild therapeutic hypothermia (MH) promotes neurogenesis in the brain and earlier expression of RNA-binding motif protein 3 (RBM3) in the cerebral cortex and hippocampus of rats. However, the mechanism underlying RBM3 regulating MH-induced neurogenesis remains unclear. This study simulated I/R injury after CA by oxygen-glucose deprivation/reperfusion (OGD/R) of mouse NSCs to determine whether RBM3 mediates the neuroprotective effects of MH in neural stem cells (NSCs) after ischemia-reperfusion (I/R) injury and whether this mechanism involves the phosphoinositide 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. The experimental results showed that the number of newborn NSCs increased significantly in the hypothermic group on days 3 and 5 after OGD/R injury compared with the normothermic group, and the Apoptosis of NSCs decreased significantly, we also found that the proportion of NSCs differentiated into neuroglial cells decreased, while the proportion of NSCs differentiated into neurons increased. In NSCs, MH increased the expression of RBM3 after OGD/R injury and activated the PI3K/Akt signaling pathway. By inhibiting this pathway, the effects of MH on promoting NSCs' proliferation and differentiation and inhibiting their Apoptosis were eliminated.

Keywords

Cardiac arrest; Ischemia-reperfusion; Mild therapeutic hypothermia; Neural stem cells; Oxygen-glucose deprivation/reperfusion; RNA-binding motif protein 3.

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