miR-148a-3p facilitates osteogenic differentiation of fibroblasts in ankylosing spondylitis by activating the Wnt pathway and targeting DKK1
Sheng W., Jiang H., Yuan H., Li S.
Prospective Study, published in Exp Ther Med (2022) — summary generated from the PubMed abstract.
Early human evidence such as case series or small samples is exploring possible benefits.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Prospective Study
- Journal
- Exp Ther Med (2022)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 35493425
- PMCID
- PMC9019766
- DOI
- 10.3892/etm.2022.11292
- Citations
- 11
Abstract (original English)
Ankylosing spondylitis (AS) is a chronic inflammatory form of arthritis. MicroRNAs (miRNAs) have been identified to serve as therapeutic targets in various inflammatory diseases. The aim of the present study was to determine the functional mechanism of miR-148a-3p on AS. Specimens were collected from AS patients and non-AS patients. Fibroblasts were delivered with the aid of miR-148a-3p inhibitor. Cell staining was performed to observe the morphological changes, calcified nodules, and mineralization degree. The binding sites of miR-148a-3p and DKK1 were predicted on the Starbase website and subsequently verified by means of dual-luciferase reporter assay. AS fibroblasts with silenced miR-148a-3p were transfected with si-DKK1. Levels of RUNX2 and Osteocalcin, DKK1 and Wnt1 protein and phosphorylation level of β-catenin were detected by means of western blot analysis. Results of the present study denoted that AS upregulated miR-148a-3p in fibroblasts to exacerbate osteogenic differentiation, resulting in increased calcified nodules and mineralization degree. Silencing miR-148a-3p could reverse the upregulation of RUNX2 and Osteocalcin in AS fibroblasts and reduce the calcified nodules and mineralization degree. miR-148a-3p targeted DKK1. DKK1 knockdown averted the effect of silencing miR-148a-3p in AS fibroblasts. In addition, silencing miR-148a-3p reversed the upregulation of Wn
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
Evidence level
Early human evidence such as case series or small samples is exploring possible benefits.
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