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1.
Cells ; 11(1)2022 01 05.
Article in English | MEDLINE | ID: mdl-35011735

ABSTRACT

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.


Subject(s)
Cell Differentiation , Heart Ventricles/pathology , Myocytes, Cardiac/pathology , Ploidies , Tetralogy of Fallot/pathology , Case-Control Studies , Cell Proliferation , Cell Size , Child , Child, Preschool , Connexin 43/metabolism , Female , Gap Junctions/metabolism , Gap Junctions/ultrastructure , Humans , Infant , Ki-67 Antigen/metabolism , Male , Myocardium/pathology , Myocardium/ultrastructure , Myocytes, Cardiac/ultrastructure
2.
Sci Rep ; 11(1): 3563, 2021 02 11.
Article in English | MEDLINE | ID: mdl-33574429

ABSTRACT

Telocytes are interstitial cells with long, thin processes by which they contact each other and form a network in the interstitium. Myocardial remodeling of adult patients with different forms of atrial fibrillation (AF) occurs with an increase in fibrosis, age-related isolated atrial amyloidosis (IAA), cardiomyocyte hypertrophy and myolysis. This study aimed to determine the ultrastructural and immunohistochemical features of cardiac telocytes in patients with AF and AF + IAA. IAA associated with accumulation of atrial natriuretic factor was detected in 4.3-25% biopsies of left (LAA) and 21.7-41.7% of right (RAA) atrial appendage myocardium. Telocytes were identified at ultrastructural level more often in AF + IAA, than in AF group and correlated with AF duration and mitral valve regurgitation. Telocytes had ultrastructural signs of synthetic, proliferative, and phagocytic activity. Telocytes corresponded to CD117+, vimentin+, CD34+, CD44+, CD68+, CD16+, S100-, CD105- immunophenotype. No significant differences in telocytes morphology and immunophenotype were found in patients with various forms of AF. CD68-positive cells were detected more often in AF + IAA than AF group. We assume that in aged AF + IAA patients remodeling of atrial myocardium provoked transformation of telocytes into "transitional forms" combining the morphological and immunohistochemical features with signs of fibroblast-, histiocyte- and endotheliocyte-like cells.


Subject(s)
Amyloidosis/immunology , Atrial Fibrillation/immunology , Heart Defects, Congenital/immunology , Telocytes/immunology , Aged , Amyloidosis/complications , Amyloidosis/pathology , Atrial Appendage/immunology , Atrial Appendage/pathology , Atrial Fibrillation/complications , Atrial Fibrillation/pathology , Female , Heart Atria/immunology , Heart Atria/pathology , Heart Defects, Congenital/complications , Heart Defects, Congenital/pathology , Humans , Immunophenotyping , Male , Middle Aged , Mitral Valve Insufficiency/immunology , Mitral Valve Insufficiency/pathology , Myocardium/immunology , Myocardium/pathology , Telocytes/pathology
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