4.4 Article

Dysregulated microRNA expression in rheumatoid arthritis families-a comparison between rheumatoid arthritis patients, their first-degree relatives, and healthy controls

期刊

CLINICAL RHEUMATOLOGY
卷 40, 期 6, 页码 2387-2394

出版社

SPRINGER LONDON LTD
DOI: 10.1007/s10067-020-05502-9

关键词

Autoimmunity; MicroRNA family; Rheumatoid arthritis; Sweden

资金

  1. Umea University
  2. Swedish Research Council [201802551]
  3. King Gustaf V's 80-Year Fund
  4. Swedish Rheumatism Association
  5. Umea University, Umea, Sweden

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Recent studies show altered expression of certain microRNAs in patients with rheumatoid arthritis and their relatives compared to healthy controls, suggesting involvement of microRNA in disease progression. The expression pattern of microRNAs in relatives partly overlaps with that of RA patients. The use of corticosteroids may influence the expression of certain microRNAs.
Objective Recent studies have demonstrated an altered expression of certain microRNAs in patients with rheumatoid arthritis (RA) as well as their first-degree relatives (FDRs) compared to healthy controls (HCs), suggesting a role of microRNA in the progression of the disease. To corroborate this, a set of well-characterized RA families originating from northern Sweden were analyzed for differential expression of a selected set of microRNAs. Method MicroRNA was isolated from frozen peripheral blood cells obtained from 21 different families and included 26 RA patients, 22 FDRs, and 21 HCs. Expression of the selected microRNAs miR-22-3p, miR-26b-5p, miR-34a-3p, miR-103a-3p, miR-142-3p, miR-146a-5p, miR-155, miR-346, and miR-451a was determined by a two-step quantitative real-time polymerase chain reaction (qRT-PCR). Statistical analysis including clinical variables was applied. Results Out of the nine selected microRNAs that previously have been linked to RA, we confirmed four after adjusting for age and gender, i.e., miR-22-3p (p = 0.020), miR-26b-5p (p = 0.018), miR-142-3p (p = 0.005), and miR-155 (p = 0.033). Moreover, a significant trend with an intermediate microRNA expression in FDR was observed for the same four microRNAs. In addition, analysis of the effect of corticosteroid use showed modulation of miR-103a-3p expression. Conclusions We confirm that microRNAs seem to be involved in the development of RA, and that the expression pattern in FDR is partly overlapping with RA patients. The contribution of single microRNAs in relation to the complex network including all microRNAs and other molecules is still to be revealed.

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