Zhu Liang, Cao Maohong, Ni Yaohui, Han Lijian, Dai Aihua, Chen Rongrong, Ning Xiaojin, Liu Xiaorong, Ke Kaifu
Department of Neurology, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, People's Republic of China.
Jiangsu Province Key Laboratory for Inflammation and Molecular Drug Target, Nantong University, Nantong, 226001, Jiangsu, People's Republic of China.
Cell Mol Neurobiol. 2017 May;37(4):607-617. doi: 10.1007/s10571-016-0397-5. Epub 2016 Jun 28.
Human transforming growth factor β-activated kinase (TAK1)-binding protein 3 (TAB3) is a regulator of NF-κB which has been mainly found in a variety of cancers. While TAB3 is highly expressed in brain tissue, little is known about the function of TAB3 in central nervous system. Our group established an animal ICH model with autologous whole blood injected into brain, and also a cell ICH model with hemin stimulation. Our Western blot result showed up-regulation of TAB3 during neuronal apoptosis in the model of intracerebral hemorrhage (ICH), which was also approved by immunofluorescence and immunohistochemistry result. Besides, increasing TAB3 level was accompanied by the increased expression of active-caspase-3, active-caspase-8, and decreased expression of Bcl-2. Furthermore, in in vitro study, the level of neuronal apoptosis was decreased by applying TAB3- RNA interference in PC12 cells. All the results above suggested that TAB3 probably participates in the process of neuronal apoptosis following ICH.
人转化生长因子β激活激酶(TAK1)结合蛋白3(TAB3)是一种核因子κB(NF-κB)调节剂,主要在多种癌症中被发现。虽然TAB3在脑组织中高表达,但关于TAB3在中枢神经系统中的功能知之甚少。我们团队建立了自体全血注入脑内的动物脑出血模型以及氯化血红素刺激的细胞脑出血模型。我们的蛋白质免疫印迹结果显示,在脑出血(ICH)模型中神经元凋亡过程中TAB3上调,免疫荧光和免疫组织化学结果也证实了这一点。此外,TAB3水平升高伴随着活性半胱天冬酶-3、活性半胱天冬酶-8表达增加以及Bcl-2表达降低。此外,在体外研究中,通过在PC12细胞中应用TAB3-RNA干扰降低了神经元凋亡水平。上述所有结果表明,TAB3可能参与脑出血后神经元凋亡过程。