Human neural stem cell secretome relieves endoplasmic reticulum stress-induced apoptosis and improves neuronal functions after traumatic brain injury in a rat model

IF 2.9 4区生物学 Q3 CELL BIOLOGY

Journal of Molecular Histology Pub Date : 2024-04-12 DOI:10.1007/s10735-024-10192-7

Yating Ling, Murugan Ramalingam, Xiaorui Lv, Dongdong Niu, Yu Zeng, Yun Qiu, Yu Si, Tao Guo, Yinying Ni, Jingwen Zhang, Ziyu Wang, Hae-Won Kim, Jiabo Hu

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Abstract

Neural stem cell secretome (NSC-S) plays an important role in neuroprotection and recovery. Studies have shown that endoplasmic reticulum stress (ER stress) is involved in the progression of traumatic brain injury (TBI) and is a crucial cause of secondary damage and neuronal death after brain injury. Whether NSC-S is engaged in ER stress and ER stress-mediated neuronal apoptosis post-TBI has not been investigated. In the study, the Feeney SD male rat model was established. The results showed that NSC-S treatment significantly improved the behavior of rats with TBI. In addition, NSC-S relieved ER stress in TBI rats and was observed by transmission electron microscopy and western blot. The specific mechanism was further elucidated that restoration was achieved by alleviating the PERK-eIF2α pathway and thus protecting neurons from apoptosis. Notably, the discovery of calumenin (CALU) in NSC-S by liquid chromatography-tandem mass spectrometry (LC–MS/MS/MS) may be related to the protective effect of NSC-S on ER stress in neurons. Also, the mechanism by which it functions may be related to ubiquitination. In summary, NSC-S improved prognosis and ER stress in TBI rats and might be a promising treatment for relieving TBI.

Graphical Abstract

Neural stem cell secretome protects neurons from apoptosis through different pathways.

Abstract Image

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人神经干细胞分泌物能缓解内质网应激诱导的细胞凋亡，改善大鼠脑外伤后的神经元功能

神经干细胞分泌组（NSC-S）在神经保护和恢复中发挥着重要作用。研究表明，内质网应激（ER应激）参与创伤性脑损伤（TBI）的进展，是脑损伤后二次损伤和神经元死亡的关键原因。NSC-S是否参与ER应激和ER应激介导的创伤性脑损伤后神经元凋亡尚未得到研究。该研究建立了 Feeney SD 雄性大鼠模型。结果表明，NSC-S 治疗可明显改善创伤性脑损伤大鼠的行为。此外，NSC-S 还能缓解创伤性脑损伤大鼠的 ER 应激，并通过透射电子显微镜和 Western 印迹进行了观察。其具体机制被进一步阐明，即通过缓解 PERK-eIF2α 通路，从而保护神经元免于凋亡。值得注意的是，液相色谱-串联质谱法（LC-MS/MS/MS）发现了NSC-S中的钙黄绿素（CALU），这可能与NSC-S对神经元ER应激的保护作用有关。此外，其发挥作用的机制可能与泛素化有关。总之，NSC-S改善了创伤性脑损伤大鼠的预后和ER应激，可能是一种有希望缓解创伤性脑损伤的治疗方法。

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来源期刊

Journal of Molecular Histology 生物-细胞生物学

CiteScore

5.90

自引率

0.00%

发文量

审稿时长

1 months

期刊介绍： The Journal of Molecular Histology publishes results of original research on the localization and expression of molecules in animal cells, tissues and organs. Coverage includes studies describing novel cellular or ultrastructural distributions of molecules which provide insight into biochemical or physiological function, development, histologic structure and disease processes. Major research themes of particular interest include: - Cell-Cell and Cell-Matrix Interactions; - Connective Tissues; - Development and Disease; - Neuroscience. Please note that the Journal of Molecular Histology does not consider manuscripts dealing with the application of immunological or other probes on non-standard laboratory animal models unless the results are clearly of significant and general biological importance. The Journal of Molecular Histology publishes full-length original research papers, review articles, short communications and letters to the editors. All manuscripts are typically reviewed by two independent referees. The Journal of Molecular Histology is a continuation of The Histochemical Journal.