Neuroprotection of netrin-1 on neurological recovery via Wnt/β-catenin signaling pathway after spinal cord injury.

Abstract:

:The neuroprotective effects of netrin-1 after spinal cord injury and its specific molecular mechanisms have not been elucidated. In our study, Western blot, transferase UTP nick end labeling staining and immunofluorescence staining first showed that netrin-1 significantly decreased the expression levels of caspase-3, caspase-9, transferase UTP nick end labeling-positive neurons, nuclear factor kappa-B, and tumor necrosis factor-α after spinal cord injury, which inhibited neuronal apoptosis and inflammatory response. Using Nissl and HE staining, we also found that netrin-1 significantly increased the number of Nissl bodies in the anterior horn of spinal cord and promoted the recovery of injured tissue after spinal cord injury, consequently providing a good microenvironment for recovery of motor function. Finally, the results of Basso, Beattie, and Bresnahan score further confirmed that netrin-1 promoted the recovery of neurological function after spinal cord injury. Furthermore, netrin-1 significantly promoted the expression of β-catenin and inhibited the expression of glycogen synthase kinase-3β, which activated Wnt/β-catenin signaling pathway after spinal cord injury. However, XAV939 inhibited Wnt/β-catenin signaling pathway, which significantly inhibited the regulatory effect of netrin-1 on apoptosis, inflammation, Nissl bodies, damaged tissues, and neuroprotection. These results demonstrate for the first time the correlation between netrin-1 and Wnt/β-catenin signaling pathway after spinal cord injury and show that netrin-1 exerts its neuroprotective effect by activating this signaling pathway after spinal cord injury.

journal_name

Neuroreport

journal_title

Neuroreport

authors

Gao K,Niu J,Dang X

doi

10.1097/WNR.0000000000001441

subject

Has Abstract

pub_date

2020-05-07 00:00:00

pages

537-543

issue

7

eissn

0959-4965

issn

1473-558X

journal_volume

31

pub_type

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