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.