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Altered expression of microRNAs targeting Dkk-1 in peripheral blood mononuclear cells of patients with ankylosing spondylitis

INTRODUCTION: Ankylosing spondylitis (AS) is a chronic inflammatory disease characterised by new bone formation, and Dickkopf homologue 1 (Dkk-1) may contribute to the ankylosis of the sacroiliac joint as a main regulator of the Wingless (Wnt) pathway. Increasing evidence shows that microRNAs target...

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Detalles Bibliográficos
Autores principales: Huang, Jinxian, Song, Guoxiang, Yin, Zhihua, Fu, Zhongchao, Zhang, Lijun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Polish Society of Experimental and Clinical Immunology 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6526586/
https://www.ncbi.nlm.nih.gov/pubmed/31114438
http://dx.doi.org/10.5114/ceji.2019.84018
Descripción
Sumario:INTRODUCTION: Ankylosing spondylitis (AS) is a chronic inflammatory disease characterised by new bone formation, and Dickkopf homologue 1 (Dkk-1) may contribute to the ankylosis of the sacroiliac joint as a main regulator of the Wingless (Wnt) pathway. Increasing evidence shows that microRNAs targeting Dkk-1 might play a critical role in the pathogenesis of rheumatic diseases. We aim to investigate alterations in expression of miRNAs targeting Dkk-1 in AS patients in this study. MATERIAL AND METHODS: The peripheral blood mononuclear cells (PBMCs) of 20 AS patients and 20 normal controls were collected in our study. Three miRNAs targeting DKK1 including miR-29a, miR-335, and miR-363 were selected and quantitative real-time PCR was used to identify the expression of the three miRNAs in these samples. Correlation analysis was conducted between altered miRNA expression and erythrocyte sedimentation rate (ESR), C-reactive protein (CRP), Bath Ankylosing Spondylitis Disease Activity Index (BASDAI), Bath Ankylosing Spondylitis Function Index (BASFI), and mSASSS (modified Stoke Ankylosing Spondylitis Spinal Score). RESULTS: The expression of miR-29a was significantly higher in AS patients than in healthy controls (p < 0.01), while no significance was observed in the expression of miR-335 and miR-363 between AS patients and healthy controls (p > 0.05). No correlation was observed between miR-29a and ESR, CRP, BASDAI, and BASFI (p > 0.05). The elevated miR-29a expression was correlated with disease duration and mSASSS (p < 0.05). CONCLUSIONS: MiR-29a might be a useful marker in AS new bone formation and contributes to the regulation of Dkk-1 in Wnt signalling.