ArticleActa endocrinologica (Bucharest, Romania : 2005)
HSA-MIR-183-3P TARGETING ATAXIA-TELANGIECTASIA MUTATED PROTEIN REGULATION OF NF-ΚB SIGNALING PATHWAY AFFECTS CELLULAR SENESCENCE CAUSED BY DNA DAMAGE IN LUMBAR DISC DEGENERATION.
Article in Acta endocrinologica (Bucharest, Romania : 2005). The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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3 authors at 1 institution in 1 country.
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Abstract
Aims: To test the effect of Hsa-miR-183-3p on cell aging and disc degeneration in lumbar intervertebral disc. Methods: This study combined clinical research with basic cell experiment, analyzing clinical data from patients with lumbar disc degeneration and traumatic lumbar spine fracture, as well as the differences in baseline data. The degree of lumbar disc injury in patients of different ages was also compared. Differentially expressed miRNAs were predicted via GEO database, and qPCR confirmation was determined by collecting cartilage endplates from two groups. ACAN, Col2A1, p16, p21, and p53 were detected by immunofluorescence, Western blot and qPCR in human nucleus pulposus cells. Changes of cell senescence were detected. The binding of Hsa-miR-183-3p to ataxia-telangiectasia mutated protein was confirmed by dual luciferase reporter assay. Results: Degenerative discs showed elevated expression of hsa-miR-183-3p, which may be upregulated by TNF-α via NF-κB signaling pathway and target ataxia-telangiectasia mutated protein regulation. Conclusion: Degeneration of the intervertebral disc can be accelerated by TNF-α. Additionally, Hsa-miR-183-3p passed NF-κB signaling pathway is blocked via up-regulation of TNF-α to reduce inflammation via targeting ataxia-telangiectasia mutated protein. As a result, this negative feedback mechanism may assist in maintaining a low degenerative load and preserving chronic disc degeneration.
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