Abstract
Far upstream element binding protein 1 (FBP1) has been identified as an upstream gene of p27kip1 (p27), which is a key regulator of mammalian cell cycle regulation and neurogenesis. To elucidate the expression and function of FBP1 in central nervous system lesion and repair, we performed a traumatic brain injury (TBI) model in adult rats. We observed that FBP1 protein level significantly reduced at day 3 after injury, and the downregulation of FBP1 was predominant in astrocytes, which were largely proliferated after injury. Furthermore, in vitro, overexpression of FBP1 was concomitant with the up-regulation of p27 and reduction of PCNA in LPS-induced astrocyte proliferation. These results suggest that a decreased level of FBP1 in brain is involved in the proliferation of glial cells after TBI.
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