ArticleClinical epigenetics2019
Suv39h1 promotes facet joint chondrocyte proliferation by targeting miR-15a/Bcl2 in idiopathic scoliosis patients.
Article in Clinical epigenetics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 1 of them a synthesis that pooled it.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
16 citing papers in PubMed, 1 synthesis or guideline pooled it, 33 citations in OpenAlex.
- Pooled it
- Circulating microRNA signatures for diagnosis and prediction of curve progression in pediatric patients with idiopathic scoliosis.Journal of orthopaedic surgery and research · 2026Article
- miRNA-130b-3p upregulation impairs osteogenic differentiation in AIS patients by inhibiting the IGF1/ERK pathway.Cellular and molecular life sciences : CMLS · 2025Article
- IL6ST participates in the development of adolescent idiopathic scoliosis by regulating bone marrow mesenchymal stem cells.Communications biology · 2025Article
- Genome-wide profiling of circulating microRNAs in adolescent idiopathic scoliosis and their relation to spinal deformity severity, and disease pathophysiology.Scientific reports · 2025Article
- Scoliosis as a Paradigm of Pathological Spinal Curvature: Molecular Mechanisms and Imaging Innovations : Molecular and Imaging Insights in Scoliosis.Galen medical journal · 2025Review
- Investigating the Differential Circulating microRNA Expression in Adolescent Females with Severe Idiopathic Scoliosis: A Proof-of-Concept Observational Clinical Study.International journal of molecular sciences · 2024Observational
- SUV39H1 is a novel biomarker targeting oxidative phosphorylation in hepatitis B virus-associated hepatocellular carcinoma.BMC cancer · 2023Article
- Advances in epigenetic research of adolescent idiopathic scoliosis and congenital scoliosis.Frontiers in genetics · 2023Review
- The Potential Role of Dysregulated miRNAs in Adolescent Idiopathic Scoliosis and 22q11.2 Deletion Syndrome.Journal of personalized medicine · 2022Review
- Upregulation of microRNA-96-5p is associated with adolescent idiopathic scoliosis and low bone mass phenotype.Scientific reports · 2022Article
- Histone Modifications and Chondrocyte Fate: Regulation and Therapeutic Implications.Frontiers in cell and developmental biology · 2021Review
- Single-Cell Integration Analysis of Heterotopic Ossification and Fibrocartilage Developmental Lineage: Endoplasmic Reticulum Stress Effector Xbp1 Transcriptionally Regulates the Notch Signaling Pathway to Mediate Fibrocartilage Differentiation.Oxidative medicine and cellular longevity · 2021Article
- High methylation of lysine acetyltransferase 6B is associated with the Cobb angle in patients with congenital scoliosis.Journal of translational medicine · 2020Article
- Emerging roles of non-coding RNAs in scoliosis.Cell proliferation · 2020Review
- Changes in circulating cell-free nuclear DNA and mitochondrial DNA of patients with adolescent idiopathic scoliosis.BMC musculoskeletal disorders · 2019Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIdiopathic scoliosis (IS) is a complex disease with an unclear etiology, and the worldwide prevalence is approximately 2-3%. As an important link between environmental factors and phenotypic differences, epigenetic changes, such as lncRNA, miRNA, and DNA methylation, have recently been reported to be associated with the development of IS. However, the correlation between histone methylation, another classical epigenetic mechanism, and IS has not been determined. In this study, we investigated the morphological changes, alterations in the levels of histone methylation, and cell proliferation-related pathway in inferior facet joint cartilage in 11 IS patients and 10 comparable controls.
resultsCompared with the control group, narrowed facet joint cartilage but increased proliferative chondrocytes and upregulated collagen type II (COL2A1) and B-cell lymphoma-2 (Bcl2) were observed in IS patients. Additionally, tri-methylation levels of H3K9 (H3K9me3) rather than other lysine sites were significantly increased in IS patients, coinciding with the upregulation of its specific enzyme, suppressor of variegation 3-9, drosophila homolog of 1 (SUV39H1). In addition, Bcl2-targeted miR-15a was downregulated in IS patients, and the level of H3K9me3 in the promoter region of the miR-15a host gene was remarkably increased in IS patients compared with the control group. Moreover, overexpressing SUV39H1 in ATDC5 cells with increased H3K9me3 levels led to similar changes, with increased expression of COL2A1 and Bcl2, decreased expression of miR-15a, and increased cell proliferation.
conclusionsThus, our study suggests that increased chondrocyte proliferation occurs in the facet joint cartilage of IS patients compared with the control group and may be promoted by the elevated levels of H3K9me3 and SUV39H1, which regulate the miR-15a/Bcl2 pathway. This dysregulation of chondrocyte proliferation could result in abnormal spinal growth and may additionally participate in the development and progression of IS.
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