ArticleJournal of orthopaedic surgery and research2019
A new single nucleotide polymorphism affects the predisposition to thoracic ossification of the posterior longitudinal ligament.
Article in Journal of orthopaedic surgery and research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Detection of differentially expressed genes in bantam chickens providing insights into chicken dwarfism.BMC genomic data · 2025Article
- Degenerative Thoracic Myelopathy: A Scoping Review of Epidemiology, Genetics, and Pathogenesis.Global spine journal · 2024Article
- The coordinated activities of collagen VI and XII in maintenance of tissue structure, function and repair: evidence for a physical interaction.Frontiers in molecular biosciences · 2024Article
- Pathogenesis of thoracic ossification of the ligamentum flavum.Frontiers in pharmacology · 2024Review
- Ossification of the posterior longitudinal ligament located on the concave side of the apex vertebra in adult spinal deformity.Nagoya journal of medical science · 2021Article
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Authors and funding
6 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundThoracic ossification of the posterior longitudinal ligament (T-OPLL) is one of the common factors that cause thoracic spinal stenosis, which results in intractable myelopathy and radiculopathy. Our previous study first reported rs201153092A site mutation in the collagen 6A1 (COL6A1) gene as a potentially pathogenic locus for T-OPLL. We aimed to determine whether the rs201153092A site mutation causes abnormal expression of the COL6A1 in Han Chinese patients with T-OPLL and whether this locus is also associated with cervical-OPLL.
methodsPeripheral blood was collected from a total of 60 patients with T-OPLL disease (30 patients carrying the rs201153092A site mutation in COL6A1 and 30 wild-type patients) and 400 northern Chinese individuals (200 cervical-OPLL patients and 200 control subjects) using the Sequenom system. The expression of COL6A1 was analyzed by enzyme-linked immunosorbent assay, reverse transcription-quantitative polymerase chain reaction, and Western blotting.
resultsrs201153092A mutation resulted in markedly increased COL6A1 gene expression levels in peripheral blood samples. The allele frequency and genotype frequency results showed that this locus is no difference between cervical-OPLL patients and controls.
conclusionsThe rs201153092A site mutation of COL6A1 can significantly increase the expression of COL6A1. The COL6A1 gene rs201153092A site polymorphism is a potential pathogenic mutation in T-OPLL disease, which may be only associated with the occurrence of T-OPLL.
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