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Upregulation of long noncoding RNA MEG3 Induced by Heat Stress Contributes to Apoptosis of Rat Cardiomyocytes via Promoting TR3 Transcription

Xinxing Wang  Zhaoli Chen  Weili Liu  Tianhui Wang  Ruifeng Duan  Yingying Li  Lingling Pu  Bingnan Deng  
【摘要】:Mitochondria play a key role in cardiomyocytes apoptosis induced by heat stress.Our previous study indicate that TR3 binding to mitochondria and induces apoptosis under stress.However,the alteration of TR3 responding environmental heat stress is far from fully understood.Our 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 cardiomyocytes.Mechanistically,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 MEG3.Moreover,TR3 transcription was upregulated via increasing its transcription factor ELK1 the resultant from c-jun upregulation in heat stress responses.Collectively,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 cardiomyocytes.Our present study provided a significant insight into understanding the alteration and role of TR3 in heat stress cardiomyocytes.

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