title: Myocardial cardiotrophin-1 is differentially induced in congenital cardiac defects depending on hypoxemia.
abstract: OBJECTIVE
  Cardiotrophin-1 (CT-1) is upregulated by hypoxemia and hemodynamic overload and is characterized by potent hypertrophic and protective properties on cardiac cells. This study aimed to investigate whether CT-1 is differentially induced in the myocardium of infants with congenital cardiac defects depending on hypoxemia.
  
  
  RESULTS
  Infants with Tetralogy of Fallot (n = 8) or with large nonrestrictive ventricular septal defect (n = 8) undergoing corrective surgery were investigated. Expression of CT-1 was assessed at mRNA and protein levels in the right atrial and ventricular myocardium. The activation of the STAT-3 and VEGF were measured. Degradation of cardiac troponin-I served as a marker of myocardial damage. CT-1 was detected in all patients with levels negatively correlating to the arterial oxygen saturation. Higher CT-1 expression in Tetralogy of Fallot patients was associated with activation of the JAK/STAT pathway and higher cardiac troponin-I degradation.
  
  
  CONCLUSIONS
  CT-1 may mediate myocardial hypertrophy and dysfunction in infants with congenital cardiac defects, particularly in those with hypoxemia.
authors.affiliation: Department of Pediatric Cardiology, Aachen University, Aachen, Germany.
authors.forename: Ruth
authors.initials: R
authors.lastname: Heying
authors.forename: Ma
authors.initials: M
authors.lastname: Qing
authors.forename: Katharina
authors.initials: K
authors.lastname: Schumacher
authors.forename: Magdalena
authors.initials: M
authors.lastname: Sokalska-Duhme
authors.forename: Jaime F
authors.initials: JF
authors.lastname: Vazquez-Jimenez
authors.forename: Marie-Christine
authors.initials: MC
authors.lastname: Seghaye
mesh_terms: D006332:Cardiomegaly / Q000209:etiology*; D016207:Cytokines / Q000235:genetics / Q000378:metabolism*; D005260:Female; D006345:Heart Septal Defects, Ventricular / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D006801:Humans; D000860:Hypoxia / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D009206:Myocardium / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D050796:STAT3 Transcription Factor / Q000378:metabolism; D015398:Signal Transduction / Q000502:physiology; D013771:Tetralogy of Fallot / Q000209:etiology / Q000378:metabolism* / Q000601:surgery; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
chemical_list: D016207:Cytokines; D012333:RNA, Messenger; D050796:STAT3 Transcription Factor; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; C092073:cardiotrophin 1