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MCM3上调与成年大鼠创伤性脑损伤后神经元凋亡相关。

Up-regulation of MCM3 Relates to Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats.

作者信息

Ji Wei, Liu Hanzhang, Liu Chun, Shao Lifei, Liu Yuankun, Fan Shaochen, Li Xiaohong, Gong Lei Lei, Zhu Shunxing, Gao Yilu

机构信息

Department of Neurosurgery, Affiliated Hospital of Nantong University, Nantong, 226001, Jiangsu, China.

Morphology Laboratory, Medical College of Nantong University, Nantong, 226001, Jiangsu, China.

出版信息

Cell Mol Neurobiol. 2017 May;37(4):683-693. doi: 10.1007/s10571-016-0404-x. Epub 2016 Jul 11.

Abstract

Minichromosome maintenance complex component 3, one of the minichromosome maintenance proteins, functions as a part of pre-replication complex to initiate DNA replication in eukaryotes. Minichromosome maintenance complex component 3 (MCM3) was mainly implied in cell proliferation and tumorigenesis. In addition, MCM3 might play an important role in neuronal apoptosis. However, the functions of MCM3 in central nervous system are still with limited acquaintance. In this study, we performed a traumatic brain injury (TBI) model in adult rats. Western blot and immunohistochemistry staining showed up-regulation of MCM3 in the peritrauma brain cortex. The expression patterns of active caspase-3 and Bax, Bcl-2 were parallel with that of MCM3. Immunofluorescent staining and terminal deoxynucleotidyl transferase-mediated biotinylated-dUTP nick-end labeling suggested that MCM3 was involved in neuronal apoptosis. In conclusion, our data indicated that MCM3 might play an important role in neuronal apoptosis following TBI. Further understanding of these insights could serve as the basis for broadening the therapeutic scope against TBI.

摘要

微小染色体维持复合物组分3是微小染色体维持蛋白之一,作为复制前复合物的一部分,在真核生物中启动DNA复制。微小染色体维持复合物组分3(MCM3)主要与细胞增殖和肿瘤发生有关。此外,MCM3可能在神经元凋亡中起重要作用。然而,MCM3在中枢神经系统中的功能仍了解有限。在本研究中,我们在成年大鼠中建立了创伤性脑损伤(TBI)模型。蛋白质免疫印迹和免疫组织化学染色显示创伤周围脑皮质中MCM3上调。活化的半胱天冬酶-3以及Bax、Bcl-2的表达模式与MCM3的表达模式平行。免疫荧光染色和末端脱氧核苷酸转移酶介导的生物素化-dUTP缺口末端标记表明MCM3参与神经元凋亡。总之,我们的数据表明MCM3可能在TBI后的神经元凋亡中起重要作用。对这些见解的进一步了解可为拓宽TBI的治疗范围奠定基础。

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