Circ-Ctnnb1 Regulates Neuronal Injury in Spinal Cord Injury through the Wnt/β-Catenin Signaling Pathway

Abstract

Study design: Spinal cord injury (SCI) rat model and cell model were established for in vivo and in vitro experiments. Functional assays were utilized to explore the role of the circRNAs derived from catenin beta 1 (mmu_circ_0001859, circ-Ctnnb1 herein) in regulating neuronal cell viability and apoptosis. Bioinformatics analysis and mechanism experiments were conducted to assess the underlying molecular mechanism of circ-Ctnnb1. Objective: We aimed to probe into the biological function of circ-Ctnnb1 in neuronal cells of SCI. Methods: The rat model of SCI and hypoxia-induced cell model were constructed to examine circ-Ctnnb1 expression in SCI through quantitative reverse transcription real-time polymerase chain reaction (RT-qPCR). Basso, Beattie and Bresnahan (BBB) score was utilized for evaluating the neurological function. Terminal-deoxynucleoitidyl Transferase Mediated Nick End labeling (TUNEL) assays were performed to assess the apoptosis of neuronal cells. RNase R and Actinomycin D (ActD) were used to treat cells to evaluate the stability of circ-Ctnnb1. Results: Circ-Ctnnb1 was highly expressed in SCI rat models and hypoxia-induced neuronal cells, and its deletion elevated the apoptosis rate of hypoxia-induced neuronal cells. Furthermore, circ-Ctnnb1 activated the Wnt/β-catenin signaling pathway via sponging mircoRNA-205-5p (miR-205-5p) to up-regulate Ctnnb1 and Wnt family member 2B (Wnt2b). Conclusion: Circ-Ctnnb1 promotes SCI through regulating Wnt/β-catenin signaling via modulating the miR-205-5p/Ctnnb1/Wnt2b axis.

Circ_0006640 transferred by bone marrow-mesenchymal stem cell-exosomes suppresses lipopolysaccharide-induced apoptotic, inflammatory and oxidative injury in spinal cord injury

“…For instance, circ-Usp10 silencing reduced proinflammatory factors section and inhibited microglial activation, as well as suppressed neuronal death in SCI via miR-152-5p/CD84 axis [ 14 ]. SCI rat models showed a high expression of circ-Ctnnb1, and deletion of circ-Ctnnb1 enhanced hypoxia-induced neuronal apoptosis through Wnt/β-catenin pathway [ 25 ]. CircPrkcsh silencing suppressed inflammatory response in TNF-α-induced astrocytes, a SCI cell model, by miR-488/Ccl2 axis [ 26 ].…”

Aucubin promoted neuron functional recovery by suppressing inflammation and neuronal apoptosis in a spinal cord injury model

“…Neuronal apoptosis is an important component of secondary injury [37]. Inhibition of neuronal apoptosis is thought to aid in neural rehabilitation and axon regeneration [39, 60]. Therefore, development of strategies to reduce neuronal apoptosis in SCI has received greater interest.…”