Conclusion
Circ-Ctnnb1 promotes SCI through regulating Wnt/β-catenin signaling via modulating the miR-205-5p/Ctnnb1/Wnt2b axis.
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. The Basso, Beattie, and Bresnahan score was utilized for evaluating the neurological function. Terminal-deoxynucleotidyl transferase mediated nick end labeling assays were performed to assess the apoptosis of neuronal cells. RNase R and actinomycin D were used to treat cells to evaluate the stability of circ-Ctnnb1.
Objective
We aimed to probe into the biological function of circ-Ctnnb1 in neuronal cells of SCI.
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 upregulate Ctnnb1 and Wnt family member 2B (Wnt2b).