Upregulation of long noncoding RNA MEG3 Induced by Heat Stress Contributes to Apoptosis of Rat Cardiomyocytes via Promoting TR3 Transcription
作者单位：Environmental Medicine LaboratoryTianjin Institute of Environmental and Operational Medicine
会议名称：《中国生物化学与分子生物学会第十二届全国会员代表大会暨2018年全国学术会议》
会议日期：2018年
学科分类：1001[医学-基础医学(可授医学、理学学位)] 100101[医学-人体解剖与组织胚胎学] 10[医学]
基 金：supported by BWS16J010 and National Natural Science Foundation of China(81372124)
关 键 词：TR3 ELK1 c-Myc MPTP Heat Stress
摘 要：Mitochondria play a key role in cardiomyocytes apoptosis induced by heat *** previous study indicate that TR3 binding to mitochondria and induces apoptosis under ***,the alteration of TR3 responding environmental heat stress is far from fully *** present study,for the first time to the best of our knowledge,discovered that environmental thermal exposure led to MEG3 upregulation,consequently upregulate ELK1 transcription and increasing TR3 transcription,in turn resulting in decline of mitochondria membrane potential(ΔΨm) and apoptosis of ***,MEG3 upregulation was attributed to heat stress-induced c-Myc expression,while ELK1 upregulation was due to the increasing translation of c-Jun induced by ***,TR3 transcription was upregulated via increasing its transcription factor ELK1 the resultant from c-jun upregulation in heat stress ***,we uncover that heat stress exposure results in c-Myc induction and MEG3 expression elevation,further promotes c-Jun translation and in turn initiates ELK1 transcripton,leading to increase of TR3 protein trancription,and decline of mitochondria membrane potential(ΔΨm) as well as apoptosis of *** present study provided a significant insight into understanding the alteration and role of TR3 in heat stress cardiomyocytes.