首页> 外文期刊>Molecular medicine reports >Changes in the expression of DNA-binding/differentiation protein inhibitors in neurons and glial cells of the gerbil hippocampus following transient global cerebral ischemia
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Changes in the expression of DNA-binding/differentiation protein inhibitors in neurons and glial cells of the gerbil hippocampus following transient global cerebral ischemia

机译:短暂性全脑缺血后沙鼠海马神经元和神经胶质细胞中DNA结合/分化蛋白抑制剂表达的变化

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摘要

Inhibitors of DNA-binding/differentiation (ID) proteins bind to basic helix-loop-helix (bHLH) transcription factors, including those that regulate differentiation and cell-cycle progression during development, and regulate gene transcription. However, little is known about the role of ID proteins in the brain under transient cerebral ischemic conditions. In the present study, we examined the effects of ischemia-reperfusion (I-R) injury on the immunoreactivity and protein levels of IDs 1-4 in the gerbil hippocampus proper Cornu Ammonis regions CA1-3 following 5 min of transient cerebral ischemia. Strong ID1 immunoreactivity was detected in the nuclei of pyramidal neurons in the hippocampal CA1-3 regions; immunoreactivity was significantly changed following I-R in the CA1 region, but not in the CA2/3 region. Five days following I-R, ID1 immunoreactivity was not detected in the CA1 pyramidal neurons. ID1 immunoreactivity was detected only in GABAergic interneurons in the ischemic CA1 region. Weak ID4 immunoreactivity was detected in non-pyramidal cells, and immunoreactivity was again only changed in the ischemic CA1 region. Five days following I-R, strong ID4 immunoreactivity was detected in non-pyramidal cells, which were identified as microglia, and not astrocytes, in the ischemic CA1 region. Furthermore, changes in the protein levels of ID1 and ID4 in the ischemic CA1 region studied by western blot were consistent with patterns of immunoreactivity. In summary, these results indicate that immunoreactivity and protein levels of ID1 and ID4 are distinctively altered following transient cerebral ischemia only in the CA1 region, and that the changes in ID1 and ID4 expression may relate to the ischemia-induced delayed neuronal death.
机译:DNA结合/分化(ID)蛋白的抑制剂与基本螺旋-环-螺旋(bHLH)转录因子结合,包括在发育过程中调节分化和细胞周期进程并调节基因转录的抑制剂。但是,关于ID蛋白在短暂性脑缺血条件下在脑中的作用知之甚少。在本研究中,我们研究了短暂性脑缺血5分钟后,缺血再灌注(I-R)损伤对沙鼠海马体Cornu Ammonis CA1-3区免疫反应和ID 1-4蛋白质水平的影响。在海马CA1-3区的锥体神经元核中检测到强ID1免疫反应。 I-R后,CA1区域的免疫反应性发生了显着变化,但CA2 / 3区域则没有变化。 I-R后五天,在CA1锥体神经元中未检测到ID1免疫反应性。仅在缺血性CA1区域的GABA能中间神经元中检测到ID1免疫反应性。在非锥体细胞中检测到弱的ID4免疫反应性,并且仅在缺血性CA1区域再次改变了免疫反应性。 I-R后五天,在缺血性CA1区域的非锥体细胞中检测到强ID4免疫反应,该细胞被识别为小胶质细胞,而非星形胶质细胞。此外,通过蛋白质印迹研究的缺血CA1区中ID1和ID4蛋白水平的变化与免疫反应性模式一致。总之,这些结果表明,仅在CA1区短暂性脑缺血后,ID1和ID4的免疫反应性和蛋白质水平会明显改变,并且ID1和ID4表达的变化可能与缺血引起的延迟性神经元死亡有关。

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