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Experimental study of miR-503 regulating the activity as well as the function of degenerated human nucleus pulposus cells of the intervertebral disc through inhibiting Wnt pathway.
- Source :
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Journal of musculoskeletal & neuronal interactions [J Musculoskelet Neuronal Interact] 2023 Mar 01; Vol. 23 (1), pp. 131-144. - Publication Year :
- 2023
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Abstract
- Objectives: To preliminarily explore miR-503 in human degenerative disc nucleus pulposus cell effects as well as mechanisms.<br />Methods: We utilized bioinformatics analysis to determine the miRNA differential expression as well as key signal pathways existing in human nucleus pulposus cells of the degenerative intervertebral discs. Human degenerative disc nucleus pulposus cell model was cultured and established in vitro . miR-503 and TNIK-related genes are knocked down and overexpressed by lentiviral infection, then we added Wnt signaling pathway agonists; CCK-8, ELISA, RT-PCR, Western blot were used to detect proliferation, apoptosis, and activity of cells.<br />Results: Bioinformatics results demonstrated that miR-503 was significantly down-regulated in human nucleus pulposus cells of the degenerated intervertebral discs. The targeted differentially expressed genes were mainly enriched in Wnt signaling pathway. However, after screening differential genes in the Wnt pathway, it was demonstrated that miR-503 mainly regulates TNIK to achieve Wnt pathway regulation. Cell experiments in vitro showed that cell activity and function were decreased while apoptosis was increased in the degenerative cell model.<br />Conclusions: miR-503 can improve the function and activity of human nucleus pulposus cells of degenerated intervertebral disc by inhibiting Wnt expression. miR-503 mainly regulates the Wnt pathway through targeted binding with TNIK.<br />Competing Interests: The authors have no conflict of interest.
Details
- Language :
- English
- ISSN :
- 1108-7161
- Volume :
- 23
- Issue :
- 1
- Database :
- MEDLINE
- Journal :
- Journal of musculoskeletal & neuronal interactions
- Publication Type :
- Academic Journal
- Accession number :
- 36856108