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Evaluation of CX3CR1 gene DNA methylation in developmental dysplasia of the hip (DDH)

INTRODUCTION AND OBJECTIVE: Developmental dysplasia of the hip (DDH) is a musculoskeletal disorder. Genetic and epigenetic changes in C-X3-C motif chemokine receptor 1 (CX3CR1) may lead to disturbance in chondrocyte development and change the labrum dimensions, which indirectly result in hip joint i...

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Detalles Bibliográficos
Autores principales: Nejadhosseinian, Mohammad, Haerian, Hoda, Shirkoohi, Reza, Karami, Jafar, Mortazavi, Seyed Mohammad Javad
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC9523927/
https://www.ncbi.nlm.nih.gov/pubmed/36175906
http://dx.doi.org/10.1186/s13018-022-03324-w
Descripción
Sumario:INTRODUCTION AND OBJECTIVE: Developmental dysplasia of the hip (DDH) is a musculoskeletal disorder. Genetic and epigenetic changes in C-X3-C motif chemokine receptor 1 (CX3CR1) may lead to disturbance in chondrocyte development and change the labrum dimensions, which indirectly result in hip joint instability. Considering the important role of this gene in cell migration, cell adhesion and bone and cartilage development, we aimed to evaluate the CX3CR1 gene methylation in DDH pathogenesis. METHODS: Our study comprised of forty-five DDH patients and forty-five healthy control subjects with healthy femoral neck cartilage. The healthy controls had total or hemiarthroplasty for the femoral neck fracture. Samples were collected from the femoral head (cartilage) of DDH patients and healthy controls. Genomic DNA was obtained from the samples, and DNA methylation of CX3CR1 gene was analyzed via metabisulfite method. RESULTS: Methylation analysis reveals no significant differences in promoter of CX3CR1 gene in cartilage samples from DDH patients and healthy control subjects (P = 0.33). CONCLUSION: Methylation status of CX3CR1 gene showed no significant difference between the patient and control groups. Our results indicate that DNA methylation may not modulate this gene in this disease and other epigenetic mechanisms such as non-coding RNAs and histone modifications could be implicated.