Cab45s inhibits neuronal apoptosis following intracerebral hemorrhage in adult rats
Cab45s inhibits neuronal apoptosis following intracerebral hemorrhage in adult rats
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Cab45s 抑制成年大鼠脑出血后的神经元凋亡。
DOI：
10.1016/j.brainresbull.2018.09.016
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发表时间：
2018-10-01
影响因子：
3.8
通讯作者：
Cao, Maohong
中科院分区：
文献类型：
--
作者：
Shen, Jiabing;Zhou, Tingting;Cao, Maohong
最近的研究表明，属于CREC家族的Cab 45可以对抗癌细胞系的凋亡。本文报道Cab 45 s在脑出血早期可能参与神经细胞凋亡的病理生理过程。我们发现，Cab 45 s的表达增强，在邻近地区的血肿后，在成年大鼠脑出血，葡萄糖调节蛋白78（GRP 78），促凋亡Bcl-2相关的X蛋白（Bax）和活性caspase-3的表达。在体外，免疫共沉淀分析表明Cab 45 s和GRP 78之间的相互作用。cab 45 s缺失可抑制氯化血红素诱导的PC 12细胞GRP 78的表达，但增加Bax和caspase-3的表达，最终促进细胞凋亡。总之，这些结果表明Cab 45 s可能对神经元凋亡发挥其抗凋亡功能。因此，本研究可能为调节Cab 45作为脑出血继发性损害的潜在可靠治疗提供证据。
Recent studies have shown that Cab45s, belonging to the CREC family, can fight against apoptosis in the cancer cell lines. Here, we report that Cab45s may involve in neuronal apoptosis at the early stage of intracerebral hemorrhage (ICH) in pathophysiology. We found that expression of Cab45s was enhanced in areas contiguous to hematoma following ICH in adult rats, and that so were the expressions of Glucose-regulated protein 78 (GRP78), pro-apoptotic Bcl-2-associated X protein (Bax) and active caspase-3. In vitro, coimmunoprecipitation analysis indicated the interaction between Cab45s and GRP78. Depletion of Cab45s attenuated the expression of GRP78, but increased the expressions of Bax and caspase-3 in PC12 cells treated with hemin, which finally promoted apoptosis. Together, these results reveal that Cab45s might exert its anti-apoptotic function against neuronal apoptosis. Thus, the study may provide evidences for regulating Cab45s as a potentially reliable treatment for the secondary damage following ICH.