4.6 Article

Expression Profiles of miR-22-5p and miR-142-3p Indicate Hashimoto's Disease and Are related to Thyroid Antibodies

Journal

GENES
Volume 13, Issue 2, Pages -

Publisher

MDPI
DOI: 10.3390/genes13020171

Keywords

miRNA; autoimmune thyroid disease; AITD; Hashimoto's thyroiditis

Funding

  1. BioPersMed COMET K [825329]
  2. MEFO Graz health 3000 [9670]

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The aim of this study was to assess the differential expression of 9 selected miRNAs related to immunological functions between patients with Hashimoto's thyroiditis (HT) and healthy controls. The results showed that miR21-5p, miR-22-3p, miR-22-5p, miR-142-3p, miR-146a-5p, miR-301-3p, and miR-451 were significantly upregulated in HT patients and altered expressions of miR-22-5p and miR-142-3p were associated with higher levels of thyroid antibodies.
Hashimoto's thyroiditis (HT) is the most prevalent autoimmune disorder of the thyroid (AITD) and characterized by the presence of circulating autoantibodies evoked by a, to date, not fully understood dysregulation of the immune system. Autoreactive lymphocytes and inflammatory processes in the thyroid gland can impair or enhance thyroid hormone secretion. MicroRNAs (miRNAs) are small noncoding RNAs, which can play a pivotal role in immune functions and the development of autoimmunity. The aim of the present study was to evaluate whether the expression of 9 selected miRNAs related to immunological functions differ in patients with HT compared to healthy controls. MiRNA profiles were analysed using quantitative reverse transcription polymerase chain reaction (qRT-PCR) in 24 patients with HT and 17 healthy controls. Systemic expressions of miR21-5p, miR-22-3p, miR-22-5p, miR-142-3p, miR-146a-5p, miR-301-3p and miR-451 were significantly upregulated in patients with HT (p similar to 0.01) and were suitable to discriminate between HT and healthy controls in AUC analysis. Altered expressions of miR-22-5p and miR-142-3p were associated with higher levels of thyroid antibodies, suggesting their contribution to the pathogenesis of HT.

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