Myocardial cardiotrophin-1 is differentially induced in congenital cardiac defects depending on hypoxemia

Future Cardiology
Ruth HeyingMarie-Christine Seghaye

Abstract

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. 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. CT-1 may mediate myocardial hypertrophy and dysfunction in infants with congenital cardiac defects, particularly in those with hypoxemia.

References

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Methods Mentioned

BETA
electrophoretic mobility shift assay
electrophoretic
biopsy
PCR
electrophoresis
protein assay
nuclear translocation

Software Mentioned

Statistical Package for Social Sciences ( SPSS
Quantity One Quantification

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