Abstract
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 3day, and then declined to basal levels at 14days 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.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.