Up-regulation of MCM3 Relates to Neuronal Apoptosis After Traumatic Brain Injury in Adult Rats |
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Authors: | Wei Ji Hanzhang Liu Chun Liu Lifei shao Yuankun Liu Shaochen Fan Xiaohong Li Lei lei Gong Shunxing Zhu Yilu Gao |
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Affiliation: | 1.Department of Neurosurgery,Affiliated Hospital of Nantong University,Nantong,China;2.Morphology Laboratory,Medical College of Nantong University,Nantong,China;3.Experimental Animal Center of Nantong University,Medical College of Nantong University,Nantong,China;4.Labortary of Surgery,Affiliated Hospital of Nantong University,Nantong,China;5.Key Laboratory of nerve Regeneration,Nantong University,Nantong,China |
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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. |
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