Galactin-3 regulation of CDC42 promotes neuronal autophagy following spinal cord injury

作者：Lei Yan, Xun Zhou, Qianqiu Li, Hongxiang Hong, Chunshuai Wu, Yong‐Jing Gao, Zhiming Cui, Guanhua Xu · 发表于：Frontiers in Cellular Neuroscience · 年份：2025 · DOI：10.3389/fncel.2025.1622825 · 被引用次数：1 · 研究领域：Autophagy in Disease and Therapy、Galectins and Cancer Biology、Spinal Cord Injury Research

Background Spinal cord injury (SCI) is a debilitating condition within the nervous system with a high disability rate and substantial economic burden. The functional recovery following SCI is enhanced by moderate levels of autophagy but hindered when autophagy becomes excessive. Galectin-3 (GAL3) has been recognized as an autophagy regulator; however, its role in SCI and its associated mechanism are largely unknown. Methods The Walsh clamping method was employed to establish a rat SCI model, while a high-concentration glutamate incubation method was used to create an in vitro model of spinal cord neuronal injury. Subsequent to establishing the injury models, the expression levels of GAL3 were detected using QPCR and Western Blot. Immunohistochemical staining was performed to determine the localization of GAL3 expression. SiR-GAL3 or GAL3 inhibitors were utilized to knock down or inhibit GAL3 expression, and behavioral analysis was conducted to assess the recovery of motor function in rats following SCI. Bioinformatics analysis was carried out to explore the mechanism of action of GAL3 post-SCI. Western Blot was used to examine the relationship between the expression levels of GAL3 and autophagy-related proteins following SCI. Sequencing analysis was performed to identify the differential gene expression in spinal cord neurons with knocked-down GAL3 compared to the control group after neural injury, aiming to investigate the mechanism of action between GAL3 and its downstream ...