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KMID : 1034820220180020225
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Molecular & Cellular Toxicology
2022 Volume.18 No. 2 p.225 ~ p.232
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MiR-214 inhibits apoptosis in thyroid epithelial follicular cells induced by amiodarone through the FASL/MAPK pathway
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Wen Jing
Deng Chaonan
Shi Lixin
Zhou Shi
Zhang Miao
Hu Xiaoli
Wang Nianxue
Luo Lijuan
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Abstract
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Background: Hashimoto's thyroiditis (HT), also known as chronic lymphocytic thyroiditis, is one of the most common autoimmune disease (AITD) in clinical practice. It is urgent to explore the mechanism of amiodarone-induced thyroid dysfunction.
Objective: This study aims to assess the expression levels of miR-214 and FasL in amiodarone contact type of HT, and the effect of miR-214 on cell viability and apoptosis and potential mechanism.
Results: We found that miR-214 was low expressed in the tissues of amiodarone-treated thyroiditis patients. MiR-214 increased the survival rate of amiodarone-induced thyroid epithelial follicular cells and inhibited apoptosis. Mechanically, we found that miR-214 could bind to FASL and regulate MAPK signaling pathway through FASL.
Conclusions: Our results suggested that miR-214 could be a potential therapeutic target for Hashimoto's thyroiditis.
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KEYWORD
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Hashimoto's thyroiditis (HT), miR-214, Thyroid epithelial follicular cells, FASL, MAPK pathway
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