Institute of Forensic Sciences, Soochow University, Suzhou, 215123, Jiangsu, China.
J Mol Neurosci. 2013 Sep;51(1):57-67. doi: 10.1007/s12031-012-9948-5. Epub 2013 Jan 13.
Cystathionine-β-synthase (CBS) catalyzes the condensation of serine with homocysteine to form cystathionine and occupies a crucial regulatory position between the methionine cycle and the biosynthesis of cysteine by transsulfuration. It was reported that CBS was a novel marker of both differentiation and proliferation for certain cell types, suggesting that CBS represents a survival-promoting protein. However, its expression and function in the central nervous system lesion are not well understood. To investigate changes of CBS after traumatic brain injury (TBI) and its possible role, mice TBI model was established by controlled cortical impact system, and the expression and cellular localization of CBS after TBI was investigated in the present study. Western blot analysis revealed that CBS was present in normal mice brain cortex. It gradually decreased, reached a valley at the third day after TBI, and then restored to basal level. Importantly, more CBS was colocalized with neuron. In addition, Western blot detection showed that the third day postinjury was also the apoptosis peak indicated by the elevated expression of caspase-3. Importantly, immunohistochemistry analysis revealed that injury-induced expression of CBS was colabeled by Bcl-2 and had no co-localization with caspase-3. These data suggested that CBS may be implicated in the apoptosis of neuron and involved in the pathophysiology of brain after TBI.
胱硫醚-β-合酶（CBS）催化丝氨酸与同型半胱氨酸缩合形成胱硫醚，在蛋氨酸循环和转硫途径合成半胱氨酸之间占据关键的调节位置。有报道称 CBS 是某些细胞类型分化和增殖的新型标志物，表明 CBS 代表一种促进生存的蛋白质。然而，其在中枢神经系统损伤中的表达和功能尚不清楚。为了研究创伤性脑损伤（TBI）后 CBS 的变化及其可能的作用，本研究采用皮质撞击系统建立了小鼠 TBI 模型，研究了 TBI 后 CBS 的表达和细胞定位。Western blot 分析显示 CBS 存在于正常小鼠大脑皮质中。它逐渐减少，在 TBI 后第 3 天达到低谷，然后恢复到基础水平。重要的是，更多的 CBS 与神经元共定位。此外，Western blot 检测显示，损伤后第 3 天也是 caspase-3 表达升高表明的细胞凋亡高峰。重要的是，免疫组化分析显示，损伤诱导的 CBS 表达与 Bcl-2 标记共定位，与 caspase-3 无共定位。这些数据表明，CBS 可能参与神经元的凋亡，并参与 TBI 后脑的病理生理学过程。
