Accelerated Growth, Differentiation, and Ploidy with Reduced Proliferation of Right Ventricular Cardiomyocytes in Children with Congenital Heart Defect Tetralogy of Fallot

Cells

Alexei I. Kim¹  Tatyana V. Sukhacheva¹  Leo A. Bockeria¹  Roman A. Serov¹  Natalia V. Nizyaeva²  Artem A. Burov²  Stanislav V. Pavlovich²  Gennady T. Sukhikh²  Aleksandr I. Shchegolev²  Yulia L. Podurovskaya²  Andrey L. Chernyaev³  Maria V. Samsonova³ 

[1] A.N. Bakulev National Medical Research Center of Cardiovascular Surgery, The Ministry of Health of Russian Federation, 121552 Moscow, Russia;National Medical Research Center for Obstetrics, Gynecology and Perinatology Named after Academician V.I. Kulakov of the Ministry of Healthcare of the Russian Federation, 117997 Moscow, Russia;Research Institute of Pulmonology, Federal Medical-Biological Agency of Russian Federation, 115682 Moscow, Russia;

关键词: tetralogy of Fallot;    children;    cardiomyocytes;    differentiation;    ploidy;    Cx43;   

DOI  :  10.3390/cells11010175

来源: DOAJ

【 摘 要 】

The myocardium of children with tetralogy of Fallot (TF) undergoes hemodynamic overload and hypoxemia immediately after birth. Comparative analysis of changes in the ploidy and morphology of the right ventricular cardiomyocytes in children with TF in the first years of life demonstrated their significant increase compared with the control group. In children with TF, there was a predominantly diffuse distribution of Connexin43-containing gap junctions over the cardiomyocytes sarcolemma, which redistributed into the intercalated discs as cardiomyocytes differentiation increased. The number of Ki67-positive cardiomyocytes varied greatly and amounted to 7.0–1025.5/10⁶ cardiomyocytes and also were decreased with increased myocytes differentiation. Ultrastructural signs of immaturity and proliferative activity of cardiomyocytes in children with TF were demonstrated. The proportion of interstitial tissue did not differ significantly from the control group. The myocardium of children with TF under six months of age was most sensitive to hypoxemia, it was manifested by a delay in the intercalated discs and myofibril assembly and the appearance of ultrastructural signs of dystrophic changes in the cardiomyocytes. Thus, the acceleration of ontogenetic growth and differentiation of the cardiomyocytes, but not the reactivation of their proliferation, was an adaptation of the immature myocardium of children with TF to hemodynamic overload and hypoxemia.

【 授权许可】

Unknown