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

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. 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. 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/ß-catenin signaling pathway via sponging mircoRNA-205-5p (miR-205-5p) to upregulate Ctnnb1 and Wnt family member 2B (Wnt2b). CONCLUSION: Circ-Ctnnb1 promotes SCI through regulating Wnt/ß-catenin signaling via modulating the miR-205-5p/Ctnnb1/Wnt2b axis.

Surgical treatment for idiopathic intervertebral disc calcification in a child: case report and review of the literature.

PURPOSE: Intervertebral disc calcification (IDC) is rare in children. Conservative treatment has been recommended for the majority of cases. We describe surgical treatment of a case of IDC with progressive neurological impairment and review the literature relevant to this rare entity and its management. METHODS: A 16-year-old boy presented with sudden onset of severe neck pain, radiating into his left shoulder. Three months later, he developed neurological symptoms and signs with a progressive motor and sensory loss of his left upper limb. RESULTS: Anterior cervical corpectomy with fusion and instrumentation was performed. Neurologic deficits completely resolved within 1 week. After 1-year follow-up, radiological images showed solid fusion and no further compression. CONCLUSION: Surgical decompression should be recommended for cases with acutely progressive and severe neurological impairments in IDC and a good result can be obtained. When surgery is needed, anterior decompression is usually used in cervical lesion, while in thoracic and lumbar area, posterior approach is suggested.