The upregulation of annexin A2 after spinal cord injury in rats may have implication for astrocyte proliferation.

Annexin A2 (ANXA2), is a member of the annexin family of proteins that exhibit Ca2+-dependent binding to phospholipids. One attractive biological function of ANXA2 is participating in DNA synthesis and cell proliferation. Previous studies have shown that ANXA2 play a role in the development of the central nervous system. However, the biological function of ANXA2 after spinal cord injury (SCI) is still with limited acquaintance. In the present study, we performed a SCI model in adult rats and investigated the dynamic changes of ANXA2 expression in the spinal cord. Western blot analysis indicated a striking expression upregulation of ANXA2 after SCI. Immunohistochemistry further confirmed that ANXA2 immunoactivity was expressed at low levels in normal condition and increased at 5day after SCI. Double immunofluorescence staining prompted that ANXA2 immunoreactivity was found in astrocytes and neurons. Interestingly, ANXA2 expression was increased predominantly in astrocytes. We also examined the expression profiles of proliferating cell nuclear antigen (PCNA), Cyclin D1 and active caspase-3 in the injured spinal cords by western blot. Co-expression of ANXA2/PCNA, ANXA2/Cyclin D1 was detected in glial fibrillary acidic protein. Importantly, double immunofluorescence staining revealed that cell proliferation evaluated by PCNA appeared in many ANXA2-expressing cells and rare caspase-3 was observed in ANXA2-expressing cells after SCI. In addition, ANXA2 knockdown in astrocytes resulted in the increase of PCNA expression after LPS stimulation, showing that ANXA2 inhibited astrocyte proliferation after inflammation. Our data suggested that ANXA2 might play important roles in CNS pathophysiology after SCI.