miRNA‑125a modulates autophagy of thyroiditis through PI3K/Akt/mTOR signaling pathway

Abstract

The present study examined the potential function and underlying mechanisms of microRNA‑125a (miR‑125a) in thyroiditis. Mice were subcutaneously administered with 100 µg porcine thyroglobulin weekly for 2 weeks to establish the thyroiditis model. Results of the in vivo study demonstrated that miR‑125a serum expression was upregulated in thyroiditis mice compared with the control group. In vitro studies were performed on a mouse macrophage cell line in which a model of thyroiditis was established using 10 ng/ml human interferon‑γ. Upregulated miR‑125a expression was achieved via mimic transfection. Increased miR‑125a expression reduced autophagy and cell proliferation, increased the apoptotic rate and the expression of pro‑inflammatory factors tumor necrosis factor‑α, interleukin (IL)‑1β, IL‑6 and IL‑18 via downregulation of the phosphoinositide 3‑kinase/protein kinase B/mammalian target of rapamycin (PI3K/Akt/mTOR) signaling pathway. PI3K inhibition enhanced the ability of miR‑125a to increase the inflammatory response in vitro via regulation of the PI3K/Akt/mTOR signaling pathway. These results suggest miR‑125a inhibited autophagy in a model of thyroiditis through the PI3K/Akt/mTOR signaling pathway.