Up-regulation of TUBA 1 B promotes astrocyte proliferation after spinal cord injury in adult rats

α-tubulin1b (TUBA1B) is one of five β Tubulin isoforms, which was high expression in proliferating HCC cells. However, the expression profiles of TUBA1B in spinal cord injury are still unclear. Hence, an acute spinal cord contusion injury (SCI) model in adult rats was established to probe the certain expression and biological function in central nervous system. Western blot analysis and immunohistochemistry both prompted us that TUBA1B expression was increased and got a peak at day 5 after spinal cord injury (SCI). TUBA1B immunoreactivity was found in astrocytes and neurons by double immunofluorescence. But we found the expression of TUBA1B was only increased predominantly in astrocytes. The colocalization of TUBA1B with PCNA was also detected in astrocytes. To further understand the role of TUBA1B in proliferation, the model of astrocyte proliferation induced by LPS was used in this experiment. Being similar to expression in vivo, TUBA1B expression was positively correlated with PCNA following LPS stimulation. Knocking TUBA1B down with siRNA can decrease PCNA expression in proliferation of astrocytes. These results suggest that TUBA1B can regulate proliferation of astrocytes after SCI. To summarize, we first uncover expression changes of TUBA1B in astrocyte after spinal cord injury, suggesting TUBA1B might be implicated in CNS pathophysiology after SCI.

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