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Mol Biol Rep ; 50(3): 2007-2014, 2023 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-36536183

RESUMEN

BACKGROUND: Celiac disease (CD) is a hereditary immune-mediated disorder, which is along with the enormous production of pro-inflammatory cytokines and the reduced level of tight junction proteins. The aim of this study was to determine the expression of TNF-α, IFN-γ, IL-18, Occludin, miR-122-5p and miR-197-3p genes in duodenal biopsies of treated CD patients in comparison to the controls. METHODS AND RESULTS: Biopsy specimens were taken from the duodenum of 50 treated CD patients (36 (72%) females and 14 (28%) males with mean age of 37.06 ± 7.02 years) and 50 healthy controls (17 (34%) females and 33 (66%) males with mean age of 34.12 ± 4.9). Total RNA was isolated, cDNA was synthesized and mRNA expression of TNF-α, IFN-γ, IL-18, Occludin, miR-122-5p and miR-197-3p were quantified by relative qPCR using B2M and U6 as internal control genes. All data were evaluated using SPSS (V.21) and GraphPad Prism (V.5). Our results showed that there was no significant difference between patients and controls for intestinal mRNA expression of TNF-α, IFN-γ, IL-18, Occludin, and miR-122-5p (p > 0.05) and the expression of miR-197-3p was significantly increased in CD patients relative to control subjects (p = 0.049). CONCLUSION: This study suggests that adherence to GFD may have a positive effect on the tight junction (TJ) permeability and in this process, miR-197-3p plays an important role. Increased expression of miR-197-3p with a final protective effect on Occludin expression can be further studied as a complement therapeutic target for Celiac disease.


Asunto(s)
Enfermedad Celíaca , MicroARNs , Adulto , Femenino , Humanos , Masculino , Enfermedad Celíaca/genética , Enfermedad Celíaca/patología , Dieta Sin Gluten , Interleucina-18/genética , MicroARNs/genética , MicroARNs/metabolismo , Ocludina/genética , Permeabilidad , ARN Mensajero/metabolismo , Uniones Estrechas/genética , Uniones Estrechas/metabolismo , Uniones Estrechas/patología , Factor de Necrosis Tumoral alfa/genética , Factor de Necrosis Tumoral alfa/metabolismo
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