MiR‑214 inhibits apoptosis in thyroid epithelial follicular cells induced by amiodarone through the FASL/MAPK pathway
MiR‑214 inhibits apoptosis in thyroid epithelial follicular cells induced by amiodarone through the FASL/MAPK pathway
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MiR™214 通过 FASL/MAPK 途径抑制胺碘酮诱导的甲状腺上皮滤泡细胞凋亡
DOI：
10.1007/s13273-021-00192-z
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发表时间：
2021
影响因子：
1.7
通讯作者：
Lijuan Luo
中科院分区：
文献类型：
--
作者：
Jing Wen;Chaonan Deng;Lixin Shi;Shi Zhou;Miao Zhang;Xiaoli Hu;Nianxue Wang;Lijuan Luo
背景资料：桥本氏甲状腺炎（HT），又称慢性淋巴细胞性甲状腺炎，是临床上最常见的自身免疫性疾病（AITD）之一。因此，探讨胺碘酮致甲状腺功能异常的机制是当务之急。目的：本研究旨在探讨miR-214和FasL在胺碘酮接触型桥本甲状腺炎（HT）中的表达水平，以及miR-214对细胞活力和凋亡的影响及其可能机制。结果：我们发现miR-214在胺碘酮治疗的甲状腺炎患者的组织中呈低表达。MiR-214增加胺碘酮诱导的甲状腺上皮滤泡细胞的存活率并抑制凋亡。在机制上，我们发现miR-214可以与FASL结合，并通过FASL调节MAPK信号通路。结论：miR-214可能是桥本甲状腺炎潜在的治疗靶点。
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 Hashimoto's thyroiditis (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.