title: [Change of cardiac mitochondrial STAT3 activity in rats with selenium deficiency and its relation with myocardial injury].
abstract: OBJECTIVE
  To study the phosphorylation activity of mitochondrial signal transducer and activator of transcription 3 (STAT3) in the myocardium of rats with selenium deficiency and its association with myocardial injury.
  
  
  METHODS
  Thirty-six rats were randomized into normal control group (n=18) and selenium deficiency model group (n=18) for feeding with normal and low-selenium chow, respectively, for 20, 30 and 40 weeks. The cardiac function of the rats was evaluated by carotid artery intubation, and the damage of cardiac mitochondria was observed under electron microscopy. The cardiac mitochondria were extracted for assessing succinate dehydrogenase and cytochrome C oxidase activities, and the protein expressions of phosphorylated and total STAT3 were detected.
  
  
  RESULTS
  Compared with the corresponding control groups, the rats in the model group showed significantly decreased cardiac function with obvious structural and functional damage of the cardiac mitochondria (P<0.05), which aggravated as the low-selenium feeding time extended (P<0.05). The rats in the model group also showed significantly decreased mitochondrial STAT3 activity (p-STAT3/STAT3) in the myocardium as the low-selenium feeding time prolonged (P<0.05). Pearson linear correlation analysis showed that the activity of cardiac mitochondrial STAT3 had positive correlations with the left ventricular systolic pressure, maximal increased rate of the left ventricular pressure, and the activities of succinate dehydrogenase and cytochrome C oxidase (P<0.01).
  
  
  CONCLUSIONS
  Selenium deficiency down-regulates the activity of mitochondrial STAT3 in rat heart to contribute to cardiac mitochondrial injury and the progression of heart failure.
authors.affiliation: Department of Cardiology, Xi'an Jiaotong University College of Medicine, Xi'an, China. mingzhang@stu.xjtu.edu.cn
authors.forename: Ming
authors.initials: M
authors.lastname: Zhang
authors.forename: Jin
authors.initials: J
authors.lastname: Wei
authors.forename: Xiaoqing
authors.initials: X
authors.lastname: Pan
authors.forename: Hu
authors.initials: H
authors.lastname: Shan
authors.forename: Rui
authors.initials: R
authors.lastname: Yan
authors.forename: Jiahong
authors.initials: J
authors.lastname: Xue
authors.forename: Yanhe
authors.initials: Y
authors.lastname: Zhu
authors.forename: Lin
authors.initials: L
authors.lastname: Lin
mesh_terms: D000818:Animals; D004032:Diet; D003576:Electron Transport Complex IV / Q000378:metabolism; D005260:Female; D006335:Heart Injuries / Q000378:metabolism; D008297:Male; D008929:Mitochondria, Heart / Q000187:drug effects* / Q000378:metabolism*; D051381:Rats; D017207:Rats, Sprague-Dawley; D050796:STAT3 Transcription Factor / Q000378:metabolism*; D012643:Selenium / Q000172:deficiency* / Q000494:pharmacology; D015398:Signal Transduction; D013385:Succinate Dehydrogenase / Q000378:metabolism
chemical_list: D050796:STAT3 Transcription Factor; C494088:Stat3 protein, rat; D013385:Succinate Dehydrogenase; D003576:Electron Transport Complex IV; D012643:Selenium