# SRPX2 exhibits neuroprotective effects in neural stem cells: inhibition of OGD/R-stimulated apoptosis and oxidative stress

## TL;DR

This study shows that SRPX2 protects neural stem cells from damage caused by hypoxic-ischemic encephalopathy by reducing cell death and oxidative stress.

## Contribution

The novel finding is that SRPX2 exerts neuroprotective effects by activating the Wnt/β-catenin pathway in hypoxic-ischemic conditions.

## Key findings

- SRPX2 improves survival of OGD/R-stimulated neural stem cells.
- SRPX2 inhibits apoptosis and oxidative stress in OGD/R-stimulated NSCs.
- SRPX2 activates the Wnt/β-catenin pathway to suppress apoptosis and oxidative stress.

## Abstract

Hypoxic-ischemic encephalopathy (HIE) is a major cause of infant morbidity as well as mortality. Neural stem cells (NSCs) is essential for brain development and function, and the role of NSCs in HIE is crucial and deserves further study. Sushi repeat-containing protein X-linked 2 (SRPX2) is a novel chondroitin sulfate proteoglycan which has multiple biological functions, such as cell growth and adhesion. However, SRPX2 is rarely reported in HIE process, and the mechanism is unclear. Herein, we aimed to uncover the role of SRPX2 in the progression of HIE. The oxygen-glucose deprivation/reoxygenation (OGD/R) model was established as a HIE cell model. We revealed that SRPX2 improves survival of OGD/R-stimulated NSCs. SRPX2 inhibited apoptosis of OGD/R-stimulated NSCs. Further data confirmed SRPX2 restrained oxidative stress of OGD/R-stimulated NSCs. Mechanically, SRPX2 activated the Wnt/beta-catenin pathway, and therefore suppressed the apoptosis as well as oxidative stress of OGD/R-stimulated NSCs. Collectively, SRPX2 suppressed apoptosis as well as oxidative stress of OGD/R-stimulated NSCs by activating Wnt/β-Catenin pathway.