Geng Zihui, Peng Fanzhen, Cheng Ziqian, Su Jingyun, Song Jinfang, Han Xu, Li Runxin, Li Xin, Cui Ranji, Li Bingjin
Jilin Provinicial Key Laoratory on Molecular and Chemical Genetic, Sencond Hospital of Jilin University, Changchun, People's Republic of China.
Engineering Lab on Screening of Antidepressant Drugs, Jilin Province Development and Reform Commission, Changchun, People's Republic of China.
FASEB J. 2025 May 15;39(9):e70606. doi: 10.1096/fj.202403417RR.
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.
脂肪酸结合蛋白7(FABP7)在星形胶质细胞中显著表达,是炎症反应的关键调节因子。越来越多的证据表明,FABP7通过调节树突棘生成在神经心理疾病中起关键作用。尽管如此,FABP7对抑郁症的影响及其潜在机制尚未完全明确。在此,我们使用慢性不可预测轻度应激(CUMS)诱导的抑郁症模型研究了FABP7的抗抑郁特性及其可能机制。我们的结果显示,CUMS诱导的抑郁样行为与海马体(HP)中FABP7蛋白水平降低有关。此外,HP中FABP7的过表达减轻了抑郁样行为,并增加了其下游靶点小窝蛋白-1(Cav-1)的表达。HP中FABP7的过表达特异性调节星形胶质细胞标志物蛋白胶质纤维酸性蛋白(GFAP)以及血脑屏障(BBB)相关蛋白水通道蛋白4(AQP4)、紧密连接蛋白5(CLDN-5)、闭合蛋白和低密度脂蛋白受体相关蛋白1(LRP1)的表达。值得注意的是,HP中FABP7的过表达也显著逆转了CUMS诱导的促炎因子白细胞介素-1β(IL-1β)和白细胞介素-6(IL-6)的上调。这种干预还导致突触后蛋白水平升高,包括突触后致密蛋白95(PSD95)和谷氨酸受体1(GluA1),以及脑源性神经营养因子(BDNF)增加和神经元树突棘密度增强。研究结果表明,FABP7通过抑制炎症、调节树突棘生成和调节BBB相关蛋白发挥抗抑郁样作用。