Survivin, a key component of the Wnt/β-catenin signaling pathway, contributes to traumatic brain injury-induced adult neurogenesis in the mouse dentate gyrus

Abstract

The enhancement of endogenous neurogenesis has been suggested in the treatment of traumatic brain injury (TBI); however, the factors that trigger the process of adult neurogenesis following TBI remain elusive. In the adult mammalian central nervous system, there are 2 neurogenic regions: the subgranular zone (SGZ) of the hippocampus and the subventricular zone (SVZ) of the lateral ventricles, both of which maintain relatively quiescent states in a stable microenvironment. However, once stimulated by intrinsic and extrinsic events, relevant signals are activated in these 2 regions. In this study, in order to explore the mechanisms behind endogenous neurogenesis following TBI, we investigated potential factors regulating this process. We observed that the expression of survivin, an anti-apoptotic protein, increased in a time-dependent manner in the hippocampus in a mouse model of TBI. In addition, the number of survivin (+) cells, as well as that of BrdU (+) cells increased in the SGZ of the dentate gyrus (DG) in the hippocampus following TBI, as shown by immunofluorescence double staining; the co-localization of survivin and BrdU was shown in the merged images. The expression of survivin was also significantly increased in the doublecortin (DCX) (+) immature neurons in the DG of the hippocampus soon after the induction of TBI. Taken together, these data confirm the connection between the expression of survivin and adult neurogenesis following TBI; our data also suggest the therapeutic potential of upregulating survivin expression as a novel strategy for the effective treatment of TBI.

Transcranial low-level laser therapy enhances learning, memory, and neuroprogenitor cells after traumatic brain injury in mice

“…25 We concentrated on two areas in the mouse brain; the subgranular layer of the hippocampal DG and the subventricular zone (SVZ) of the lateral ventricle. 26,27 Both these areas of the rodent brain are well known to give rise to neuroprogenitor cells both after TBI 28 and after other interventions that have been tested for possible neuroprotective and neuroregenerative effects. 29,30 The two time points of analysis were 7 days and 28 days after the TBI induction.…”

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“…Other than these increase in gene expression of Wnt-1, nucleolin, mTOR (NT NCs) and PI3K (Tar NCs) MAPK (Tar NCs) was also observed. Since survivin is known to be a key component of both MAPK/ERK and Wnt/β catenin signalling pathway [67,68], activation of these pathways could be the reason for upregulation of survivin in the tumors ( Figure 8B). …”

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“…Moreover, Zhang et al [75] suggested that there is a connection between the expression of survivin and adult neurogenesis. Thus, the observed decrement in survivin expression might be attributed to the decreased neurogenesis due to DA depletion [71] .…”