PCBP2 Modulates Neural Apoptosis and Astrocyte Proliferation After Spinal Cord Injury

星形胶质细胞 共域化 生物 细胞凋亡 中枢神经系统 基因敲除 脊髓损伤 脊髓 细胞生物学 免疫印迹 神经科学 生物化学 基因
作者
Xingxing Mao,Jin Liu,Chen Chen,Weidong Zhang,Rong Qian,Xinlei Chen,Hongjian Lu,Jianbing Ge,Chengjin Zhao,Dongmei Zhang,Youhua Wang
出处
期刊:Neurochemical Research [Springer Science+Business Media]
卷期号:41 (9): 2401-2414 被引量:21
标识
DOI:10.1007/s11064-016-1953-6
摘要

PCBP2, a member of the poly(C)-binding protein (PCBP) family, plays a pivotal role in posttranscriptional and translational regulation by interacting with single-stranded poly(C) motifs in target mRNAs. It is reported that several PCBP family members are involved in human malignancies. However, the distribution and function of PCBP2 in the central nervous system (CNS) remain unclear. In this study, we performed an acute spinal cord injury (SCI) model in adult rats and investigated the dynamic changes of PCBP2 expression in the spinal cord. Western blot and immunohistochemistry analysis revealed that PCBP2 presented in normal spinal cord. It gradually increased, reached a peak at 3 day, and then declined to basal levels at 14 days after SCI. We observed that the expression of PCBP2 was enhanced in the gray and white matter. Immunofluorescence indicated that PCBP2 was located in the neurons and astrocytes. Moreover, colocalization of PCBP2/active caspase-3 was detected in neurons, and colocalization of PCBP2/proliferating cell nuclear antigen was detected in astrocytes after SCI. These results indicated that PCBP2 might play an important role in neuronal apoptosis and astrocyte proliferation. In vitro, PCBP2-specific siRNA-transfected neuron showed significantly decrease of neuronal apoptosis and expression of cell cycle related proteins following glutamate stimulation. Meanwhile, PCBP2 knockdown also reduced primary astrocytes proliferation. All above indicated that PCBP2 might play a crucial role in cell proliferation and apoptosis. Collectively, our data suggested that PCBP2 might play important roles in CNS pathophysiology after SCI.
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