BTEB2 prevents neuronal apoptosis via promoting bad phosphorylation in rat intracerebral hemorrhage model.
BTEB2 prevents neuronal apoptosis via promoting bad phosphorylation in rat intracerebral hemorrhage model.
复制标题
BTEB2 通过促进大鼠脑出血模型中的不良磷酸化来防止神经元凋亡
DOI：
10.1007/s12031-014-0305-8
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发表时间：
2015-01
期刊：
影响因子：
--
通讯作者：
Gu J
中科院分区：
文献类型：
--
作者：
Liu X;Yuan D;Nie X;Shen J;Yan Y;Zhang D;Gu J
KRüppel样锌指转录因子5(KLF5)，又称BTEB2或IKLF，具有多种生物学功能，涉及细胞的增殖、发育和凋亡。以往的研究表明，BTEB2在食道癌和非小细胞肺癌(NSCLC)等多种疾病中具有抗凋亡作用。然而，BTEB2在中枢神经系统疾病中的分布和功能尚不清楚。在这项研究中，我们发现BTEB2在脑出血(ICH)的病理生理过程中下调神经细胞的凋亡。通过行为学测试建立大鼠脑出血模型。Western印迹和免疫组织化学显示脑出血后血肿周围BTEB2表达明显上调。双标免疫荧光显示BTEB2主要与神经元共存，少数与活化的星形胶质细胞和小胶质细胞共存。此外，我们还检测到神经元凋亡标记物活性caspase-3与BTEB2具有共定位。此外，在体外，KLF5基因敲除导致神经元凋亡增加，同时减少了Ser112和Ser136残基的Bad磷酸化。我们的研究结果提示，BTEB2通过促进脑出血后Bad的磷酸化而下调神经元的凋亡。本文的在线版本(doi：10.1007/s12031-0140305-8)包含补充材料，授权用户可以使用。
Krüppel-like zinc-finger transcription factor 5 (KLF5), known as BTEB2 or IKLF, has several biological functions that involve cell proliferation, development and apoptosis. Previous studies demonstrated that BTEB2 had anti-apoptotic effect in multiple diseases such as esophageal cancer and non-small cell lung cancers (NSCLCs). However, the distribution and function of BTEB2 in CNS diseases remain unknown. In this study, we show that BTEB2 down-regulates neuronal apoptosis during pathophysiological processes of intracerebral hemorrhage (ICH). A rat ICH model was established by behavioral tests. Western blot and immunohistochemistry revealed a remarkable up-regulation of BTEB2 expression surrounding the hematoma after ICH. Double-labeled immunofluorescence showed BTEB2 was mostly co-localized with neurons, rarely with activated astrocytes and microglia. Furthermore, we detected that neuronal apoptosis marker active caspase-3 had co-localizations with BTEB2. In addition, KLF5 knockdown in vitro specifically resulted in increasing neuronal apoptosis coupled with reduced Bad phosphorylation at both ser112 and ser136 residues. All our findings suggested that BTEB2 down-regulated neuronal apoptosis via promoting Bad phosphorylation after ICH. The online version of this article (doi:10.1007/s12031-014-0305-8) contains supplementary material, which is available to authorized users.
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影响因子：
3.7
作者：
Horne AW;Brown JK;Nio-Kobayashi J;Abidin HB;Adin ZE;Boswell L;Burgess S;Lee KF;Duncan WC
通讯作者：
Duncan WC
影响因子：
3.2
作者：
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影响因子：
14.9
作者：
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通讯作者：
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影响因子：
8.3
作者：
Hua, Y;Schallert, T;Xi, GH
通讯作者：
Xi, GH