细胞凋亡
标记法
免疫印迹
半胱氨酸蛋白酶12
半胱氨酸蛋白酶3
蛛网膜下腔出血
体内
发病机制
医学
半胱氨酸蛋白酶
生物
下调和上调
细胞生物学
内质网
病理
内科学
程序性细胞死亡
分子生物学
半胱氨酸蛋白酶-9
免疫学
生物化学
基因
遗传学
作者
Hua Li,Jing Yu,Huasheng Zhang,Yiqing Yang,Linke Huang,Dingding Zhang,Chun-Hua Hang
标识
DOI:10.1007/s11064-016-2076-9
摘要
Convincing evidences have proved that apoptosis plays a vital role in the pathogenesis of early and delayed brain injury following subarachnoid hemorrhage (SAH). Recently, a novel caspase-12-mediated apoptotic pathway has been reported to be induced by excess endoplasmic reticulum (ER) stress. Extensive protein damage occurs after SAH, which may trigger ER stress-associated apoptotic pathway. Thus, we hypothesized that caspase-12, as the major molecular marker of this novel apoptotic pathway, may be activated and involved in the pathogenesis of apoptotic injury after SAH. This study sought to investigate the changes of caspase-12 expressions in both in vitro and in vivo SAH models. Western blot analysis found significantly increased protein expressions of both pro- and active forms of caspase-12 after SAH. Quantitative real-time PCR and immunohistochemistry assays confirmed elevated caspase-12 level after SAH in vivo. Further, double immunofluorescence staining revealed obvious caspase-12 over-expression in both cortical neurons and astrocytes. Moreover, immunofluorescent co-staining in vivo demonstrated that neural cells with high immunoreactivity of caspase-12 also expressed caspase-3, and dual-immunofluorescent staining for caspase-12 and TUNEL in vitro showed that TUNEL-positive cells were more likely to exhibit higher caspase-12 immunoreactivity, indicating a potential contribution of caspase-12 activation to apoptosis in SAH. Collectively, our results showed significant upregulation of caspase-12 expression after experimental SAH. These findings also offer important implications for further investigations of the therapeutic potential of caspase-12 associated apoptosis in SAH.
科研通智能强力驱动
Strongly Powered by AbleSci AI