Abstract
The treatment of traumatic brain injury (TBI) remains a challenge due to limited knowledge about the mechanisms underlying neuronal regeneration. This current study compared the expression of WNT genes during regeneration of injured cortical neurons. Recombinant WNT3A showed positive effect in promoting neuronal regeneration via in vitro, ex vivo, and in vivo TBI models. Intranasal administration of WNT3A protein to TBI mice increased the number of NeuN+ neurons without affecting GFAP+ glial cells, compared to control mice, as well as retained motor function based on functional behavior analysis. Our findings demonstrated that WNT3A, 8A, 9B, and 10A promote regeneration of injured cortical neurons. Among these WNTs, WNT3A showed the most promising regenerative potential in vivo, ex vivo, and in vitro.
Highlights
Traumatic brain injury (TBI) is a major cause of morbidity and lifelong disability, making it a critical healthcare concern worldwide
White dashed lines indicate the borders of the injured gap
The relative intensity of glial fibrillary acidic protein (GFAP) at the proximal region over distal region was higher in phosphate buffered saline (PBS)-treated group compared to that of sham-treated group, and was higher in WNT3A-treated group compared to that of sham-treated group (Figure 4C). These results suggest that the main effect of WNT3A is on NeuN+ neurons, instead of GFAP+ cells
Summary
Traumatic brain injury (TBI) is a major cause of morbidity and lifelong disability, making it a critical healthcare concern worldwide. An estimated 69 million individuals per year suffer from TBI, and according to the Centers for Disease Control and Prevention, it accounts for over 30% of injury-related deaths in the United States [1,2,3]. The medical burden of TBI highlights the pressing need to develop better treatments for brain injury. Aberrant WNT signaling has previously been implicated in Alzheimer’s disease and Parkinson’s. We determined the expression of a number of WNT genes during regener7a]t.ioAnbeorrfanint WjuNreTdsicgonratliincaglhnasepurreovniosu. We determined the expression of a number of WNT genes during potentiarlegoefnWeraNtiTon3Aofuipnjounretdracuormticaatlicnbeurraoinnsi.nIjnurvyit.ro and in vivo studies examined the regenerative potential of WNT3A upon traumatic brain injury
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