spinal cord tissue; lesion epicenter; spinal fibroblasts
293 T; BV2
other disease animal model
TGF-beta/SMAD (promotes); fibrosis (promotes); apoptosis (promotes); inflammation (promotes); immune regulation (promotes); ceRNA regulation (other); other pathway/process (other)
Back-Splice Junction PCR / divergent primers PCR; Sanger Sequencing; RT-qPCR; RNA-seq; Transfection; Luciferase Reporter Assay; IF (Immunofluorescence); IHC (Immunohistochemistry); TUNEL; In Vivo Animal Model; H&E Staining; Western Blot; Bioinformatics Analysis
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This study identifies mouse CDR1as as a down-regulated circRNA in the lesion epicenter after spinal cord injury and validates its expression by qRT-PCR and junction sequencing. Functionally, inhibiting CDR1as reduces spinal fibrotic scarring, inflammation, apoptosis, glial activation, and Smad2/3 phosphorylation while improving neural repair and locomotor recovery. Mechanistically, CDR1as is proposed to act through the miR-7a-5p/TGF-betaR2 axis to regulate TGF-beta/Smad signaling in spinal fibrosis.
0.7795
CircRNA CDR1as affects functional repair after spinal cord injury and regulates fibrosis through the SMAD pathway.
biological research