Effect and Molecular Mechanism of Wnt/β-Catenin Signaling Pathway on Apoptosis after Spinal Cord Injury

doi:10.13188/2332-4139.1000042

Cited by 1 publication

(2 citation statements)

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“…Secondary injury plays a critical role in SCI and is induced by various factors, such as apoptosis, oxidative stress, and the inflammatory immune response (Lu et al, 2016). It has been observed that when the Wnt/β-catenin signalling pathway is activated, nerve cell apoptosis is inhibited; when the Wnt/β-catenin signalling pathways are suppressed, the nerve cell apoptosis levels increased significantly (Gao & Zhang, 2018). After SCI, the Wnt/βcatenin signalling pathway is activated, β-catenin dissociates from the APC/Axin/GSK-3β complexes and receives upstream molecular signals.…”

Section: Discussionmentioning

confidence: 99%

“…After SCI, the Wnt/βcatenin signalling pathway is activated, β-catenin dissociates from the APC/Axin/GSK-3β complexes and receives upstream molecular signals. The protein then transports the signals to the nucleus to activate the target gene, ultimately promoting axonal regeneration and accelerating the nerve function recovery process (Gao et al, 2016;Gao et al, 2015;Gao & Zhang, 2018;Lu et al, 2016;Shen et al, 2017) via the Wnt/β-catenin signalling. All these recent studies have identified the molecular mechanisms in SCI repair process via the Wnt/β-catenin signalling.…”

Section: Discussionmentioning

confidence: 99%

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Improved β-catenin detection in spinal cord tissue sections: autofluorescence quenching

2020

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Experimental studies on spinal cord regeneration are focusing on the windows of opportunity to improve spinal cord microenvironment via spinal-centric repair pathways. One pathway of particular interest is the Wnt/β-catenin signalling pathway which plays a vital role in axonal guidance, synaptic assembly and function, neuronal survival and connectivity after spinal cord trauma to induce repair. Upregulation of β-catenin expression is often taken as evidence of regeneration mechanisms through the Wnt/ β-catenin pathway. However, these studies may not have optimised the staining protocol for β-catenin to enable accurate detection of the protein. Given possible issues with the background or endogenous tissue autofluorescence, there is a need to optimise the protocol further to allow better visualisation of β-catenin. So far, there are no studies which report optimising spinal cord tissues for β-catenin to reduce autofluorescence, and as β-catenin is widely used in spinal cord injury (SCI) and other spinal cord tissue studies, thus it is an important issue to address. To achieve reliable detection and localisation of β-catenin, we utilised sequential quenching techniques using 1% NaBH4 and 1mM CuSO4 in 50mM ammonium acetate buffer to reduce both background and fixative-induced autofluorescence. Our results showed that sequential autofluorescence quenching is crucial in β-catenin detection, and this improved technique indicates that β-catenin is localised in the spinal cord white matter regions. Objective approach for the β-catenin localisation is highly significant as it unravelled an objective identification and illuminate the pattern of distribution of β-catenin for researcher focusing on spinal cord repair studies via the Wnt/β-catenin pathway following SCI.

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Section: Discussionmentioning

confidence: 99%