MicroRNA-216a-5p Regulates Hashimoto’s Thyroiditis by Targeting KIAA0101

Wei Lv, Fei Jing, Chong Geng, Na Chen

Article ID: 7208
Vol 37, Issue 3, 2023
DOI: https://doi.org/10.23812/j.biol.regul.homeost.agents.20233703.153
Received: 8 April 2023; Accepted: 8 April 2023; Available online: 8 April 2023; Issue release: 8 April 2023

Abstract

Background: MicroRNAs (miRNA) are biomarkers and potential therapeutic targets for autoimmune diseases, including Hashimoto’s thyroiditis (HT). However, there are limited studies to evaluate the mechanism of microRNAs associated with HT. This study explores the mechanism of action and anti-inflammation activity of miR-216a-5p in thyroid follicular epithelial cells. Methods: In this research, 100 ng/mL LPS (lipopolysaccharide) was used to induce Nthy-ori 3-1 cells to simulate HT in vitro, and then the cell activity and cytotoxicity were measured using CCK-8 (Cell Counting Kit-8) and flow cytometry. The KIAA0101 and miR-216a-5p expressions in the thyroid follicular epithelial cells and HT patients were measured by quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) and western blot assay. Luciferase activity was used to characterize the interaction between miR-216a-5p and KIAA010. In addition, the ability of thyroid follicular epithelial cells to secrete inflammatory factors was measured using an enzyme-linked immunosorbent assay (ELISA) kit. Results: The expression of miR-216a-5p was abnormally down-regulated in the lipopolysaccharide (LPS)-induced thyroid follicular epithelial cells and the thyroid gland of HT patients. Down-regulation of miR-216a-5p severely inhibited the proliferation activity of cells, induced apoptosis, and enhanced the inflammatory response. In addition, LPS significantly up-regulated KIAA0101 expression (p < 0.05) in HT patients. miR-216a-5p overexpression substantially inhibited KIAA0101 expression due to the existence of binding sites between miR-216a-5p and KIAA0101, enhanced cell proliferation, inhibited apoptosis and exerted anti-inflammatory activity. Furthermore, its overexpression significantly reduced the level of inflammatory factors such as tumor necrosis factor-alpha (TNF-α) and interleukin 1 beta (IL-1β) (p < 0.05). Conclusions: miR-216a-5p could bind with KIAA0101 and regulate KIAA0101 to achieve effective therapy for Hashimoto’s thyroiditis.


Keywords

miRNA;miR-216a-5p;KIAA0101;Hashimoto’s thyroiditis;autoimmune diseases


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