Astrocytic FABP7 Alleviates Depression-Like Behaviors of Chronic Unpredictable Mild Stress Mice by Regulating Neuroinflammation and Hippocampal Spinogenesis.

星形胶质细胞 FABP7 通过调节神经炎症和海马棘形成来缓解慢性不可预测轻度应激小鼠的抑郁样行为

阅读:4
作者:Geng Zihui, Peng Fanzhen, Cheng Ziqian, Su Jingyun, Song Jinfang, Han Xu, Li Runxin, Li Xin, Cui Ranji, Li Bingjin
Fatty acid binding protein 7 (FABP7) is prominently expressed in astrocytes and is a critical regulator of inflammatory responses. Accumulating evidence suggests that FABP7 is crucial in neuropsychological disease through the modulation of spinogenesis. Nonetheless, the impact of FABP7 on depressive disorders and the underlying mechanisms is not fully understood. Here, we investigated the antidepressant properties of FABP7 using the chronic unpredictable mild stress (CUMS)-induced model of depression and possible mechanisms. Our results revealed that depressive-like behavior induced by CUMS was associated with decreased levels of FABP7 protein in the hippocampus (HP). Furthermore, the overexpression of FABP7 in the HP mitigated the depressive-like behavior and increased the expression of its downstream target caveolin-1 (Cav-1). FABP7 overexpression in the HP specifically regulates the expression of the astrocyte marker protein GFAP, as well as the blood-brain barrier (BBB)-associated proteins AQP4, CLDN-5, occludin, and LRP1. Notably, the CUMS-induced upregulation of the pro-inflammatory factors IL-1β and IL-6 was also significantly reversed by FABP7 overexpression in the HP. This intervention also led to increased levels of postsynaptic proteins, including PSD95 and GluA1, as well as an increase in brain-derived neurotrophic factor (BDNF) and enhanced neuronal dendritic spine density. The findings indicate that FABP7 exerts antidepressant-like properties by inhibiting inflammation, regulating spinogenesis, and modulating BBB-related proteins.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。