The Expression Of CAP1 After Traumatic Brain Injury And Its Role In Asteocyte Proliferation

Objective To investigate the expression and localization changes of Cyclaseassociated protein 1(CAP1) in the brain cortex after traumatic brain injury and clarify the role of CAP1 in the processes of central nervous system(CNS) injury.Methods Sprague-Dawley(SD) rats were subjected to traumatic brain injury. Expression patterns of CAP1 were observed in the injured cortex by RT-PCR, Western Blot, immunohistochemistry and the distribution of CAP1 was detected by double immunofluorescence labeling assay.In vitro, primary rat astrocytes were prepared. Then, inflammatory activation model was constructed by LPS. The expression patterns of CAP1, PCNA and other related proteins were detected at different time point by Western Blot to clear the correlation between CAP1 with astrocyte proliferation.By using CAP1 specific siRNA to knock down the expression of CAP1 of astrocytes in the inflammatory activation model, we further clarify the effect of CAP1 on the proliferation of astrocytes after brain injury through the cell proliferation and cell cycle test.Results1. In the rat traumatic brain injury model, Western Blot results showed that the expression of CAP1 in cerebral cortex began to increase at 12 h, and reached the peak at 7d; immunohistochemistry results also showed an identical increase of CAP1 in injured group. Double immunofluorescence labeling analysis showed that CAP1 was mainly increased in astrocytes. At the same time, CAP1 was co-localization with Ki-67 in astrocytes.2. In vitro, after treating primary astrocytes with LPS at different time points, we found the expression of PCNA and cell cycle related proteins were gradually increased. During this process, the expression of CAP1 was also gradually increased.3. Silencing CAP1 by specific siRNA inhibited astrocytes growth and cell cycle partly.Conclusions After traumatic brain injury, the expression of CAP1 is upregulated mainly in astrocytes. CAP1 may be involved in the activation and proliferation of astrocytes during the process of traumatic brain injury.