Yin Qi, Shao Hua, Chai Jingxin, Dang Shanshan, Wang Fengjun
Department of Neurology, Harbin Medical University Affiliated Fourth Hospital, Harbin, Heilongjiang, P.R. China.
Cell Biochem Biophys. 2025 May 31. doi: 10.1007/s12013-025-01786-3.
Six-transmembrane epithelial antigen of prostate 4 (Steap4) has been suggested as a potential marker for reactive astrocytes. This investigation focuses on the role of Steap4 in ischemic stroke (IS) and its regulator in this context. A mouse model of IS was generated using middle cerebral artery occlusion (MCAO). Additionally, mouse astrocytes that underwent oxygen-glucose deprivation (OGD) were utilized for in vitro investigations. Steap4 was found to be upregulated in the brain of MCAO-challenged mice and OGD-challenged astrocytes. Steap4 silencing reduced infarct size and alleviated IS-associated pathological exacerbations in mice, as well as ameliorated A1 skewing of astrocytes and inflammatory cytokine secretion both in vivo and in vitro. Lysine demethylase 5B (Kdm5b), identified as an upstream regulator of Steap4, was poorly expressed in IS/OGD models. Kdm5b overexpression repressed Steap4 transcription by removing H3K4me3 modification, thus alleviating pro-inflammatory activation of astrocytes and neuroinflammation. However, Kdm5b's protective effects were diminished upon Steap4 restoration in mice or astrocytes. In conclusion, this study suggests that the loss of Kdm5b leads to aberrant upregulation of Steap4, contributing to pro-inflammatory activation of astrocytes and brain damage in IS.
前列腺六次跨膜上皮抗原4(Steap4)已被认为是反应性星形胶质细胞的潜在标志物。本研究聚焦于Steap4在缺血性中风(IS)中的作用及其在此背景下的调节因子。采用大脑中动脉闭塞(MCAO)建立IS小鼠模型。此外,利用经历氧葡萄糖剥夺(OGD)的小鼠星形胶质细胞进行体外研究。发现Steap4在MCAO攻击的小鼠大脑和OGD攻击的星形胶质细胞中上调。Steap4沉默可减小小鼠梗死面积,减轻IS相关的病理恶化,还可改善体内外星形胶质细胞的A1偏移和炎性细胞因子分泌。赖氨酸去甲基化酶5B(Kdm5b)被确定为Steap4的上游调节因子,在IS/OGD模型中表达较低。Kdm5b过表达通过去除H3K4me3修饰抑制Steap4转录,从而减轻星形胶质细胞的促炎激活和神经炎症。然而,在小鼠或星形胶质细胞中恢复Steap4后,Kdm5b的保护作用减弱。总之,本研究表明Kdm5b的缺失导致Steap4异常上调,促成IS中星形胶质细胞的促炎激活和脑损伤。