Loss of SV2A promotes human neural stem cell apoptosis via p53 signaling

Hongxiang Yu; Yingying Han; Can Cui; Gang Li; Bei Zhang

doi:10.1016/j.neulet.2023.137125

Loss of SV2A promotes human neural stem cell apoptosis via p53 signaling

Neurosci Lett. 2023 Mar 13:800:137125. doi: 10.1016/j.neulet.2023.137125. Epub 2023 Feb 11.

Authors

Hongxiang Yu¹, Yingying Han¹, Can Cui¹, Gang Li², Bei Zhang³

Affiliations

¹ Department of Neurology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200092, China.
² Department of Neurology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200092, China. Electronic address: ligang@tongji.edu.cn.
³ Department of Neurology, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai 200092, China. Electronic address: zhangbei0227@163.com.

PMID: 36780942
DOI: 10.1016/j.neulet.2023.137125

Abstract

This study investigated the role of synaptic vesicle protein 2A (SV2A) in the regulation of human induced pluripotent stem cell-derived neural stem cells (NSCs). SV2A was highly expressed in NSCs. SV2A knockdown promotes apoptosis, which was associated with an upregulation of genes involved in p53 signaling as determined by transcriptome analysis. Treatment with the small molecule p53 inhibitor pifithrin-α reversed the promotion of NSC apoptosis induced by loss of SV2A. These results demonstrate that SV2A plays an important role in regulating NSC survival via the p53 signaling pathway.

Keywords: Apoptosis; Neural stem cell; P53 signaling pathway; Synaptic vesicle protein 2A.

Publication types

Research Support, Non-U.S. Gov't

MeSH terms

Apoptosis
Humans
Induced Pluripotent Stem Cells* / metabolism
Membrane Glycoproteins / metabolism
Nerve Tissue Proteins / metabolism
Neural Stem Cells* / metabolism
Signal Transduction
Tumor Suppressor Protein p53 / metabolism

Substances

Tumor Suppressor Protein p53
SV2A protein, human
Membrane Glycoproteins
Nerve Tissue Proteins