MCM7 expression is altered in rat after spinal cord injury.

Minichromosome maintenance protein 7 (MCM7), a member of the minichromosome maintenance protein family, is essential for eukaryotic DNA replication initiation and the early stage of the elongation process. MCM7 participates in the cell cycle control of genome duplication. While it is ubiquitously expressed in all tissues, the biological function of MCM7 in the central nervous system is still with limited acquaintance. In the present study, we performed a spinal cord injury (SCI) model in adult rats. Western blotting indicated a marked alteration of MCM7 after SCI. Immunohistochemistry analysis revealed a wide distribution of MCM7 in the spinal cord. Double immunofluorescence staining showed that MCM7 immunoreactivity was increased predominantly in neurons, astrocytes, and microglia after SCI. We also examined the expression profiles of active caspase-3, proliferating cell nuclear antigen (PCNA), and Ki67, whose changes were correlated with the expression profiles of MCM7. Moreover, colocalization of MCM7/active caspase-3 was detected in neuronal nuclei (NeuN), and colocalization of MCM7/PCNA was detected in NeuN, glial fibrillary acidic protein, and CD11b, respectively. Our results suggest that MCM7 might be implicated in the apoptosis of neuron and proliferation of astrocytes and microglia after SCI.

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