Author/Editor     Petrovič, Danijel; Zorc-Pleskovič, Ruda
Title     Programmed cell death and proliferation of the cardiomyocytes in the heart failure
Type     članek
Source     In: Pajer Z, Štiblar-Martinčič D, editors. International symposium on cardiovascular diseases. Proceedings of the 29th memorial meeting devoted to prof. dr. Janez Plečnik; 1998 Dec 3-5; Ljubljana. Ljubljana: Medical faculty, Institute of histology and embryology,
Publication year     1998
Volume     str. 385-91
Language     eng
Abstract     Heart failure is the final clinical manifestation of a variety of cardiovascular diseases, such as coronary artery disease (CAD), hypertension, valvular heart disease (VHD), myocarditis, dilated cardiomyopathy (DCM), and alcohol abuse. Apoptosis of myocytes, molecular regulators of apoptosis (p53 and bcl-2), and proliferating markers (K-67 and proliferating cell nuclear antigen-PCNA) were studied inthe patients with heart failure of different etiologies. Right ventricle endomyocardial samples of 12 patients with terminal heart failure due to DCM, 10 patients with ischemic cardiomyopathy, 8 patients with VHD (mitral and tricuspid insufficency) were taken during operation, analyzed studied and compared with 10 traffic accident victims. The patients were in the NYHA class III or IV. TUNEL method was used for the detection of apoptosis. Immunohistochemical staining formolecular regulators of apoptosis, p53 and BCL-2, was performed with avidin-biotin complex techniques. Additionally, the expression of a molecular indicatior of the activation of cell cycle, PCNA and Ki-67, was examined. Apoptosis of cardiomyocytes was present in 0.08 percent of myocytes in DCM, but not in heart failure due to CAD and valvular heart disease. Apoptosis of cardiomyocytes was not p53-dependent. Incrased expression of bcl-2 was found in the patients with heart failure of different etiologies compared to controls. PCNA labeling involved more than 3.0 percent of myocytes in the heart failure compared with 1.2 percent in the control group. MIB labeling involved 0.1 percent of myocytes in DCM, but no MIB-positive myocytes were found in the heart failure of other etiologies and in the control group. The volume density of interstitum was 23% in DCM, 22% in valvular heart disease, 21% in CAD, and 10% in the control group.(Abstract truncated at 2000 characters)
Descriptors     HEART FAILURE, CONGESTIVE
APOPTOSIS
CARDIOMYOPATHY, CONGESTIVE
PROLIFERATING CELL NUCLEAR ANTIGEN
DNA NUCLEOTIDYLEXOTRANSFERASE
PROTO-ONCOGENE PROTEINS C-BCL-2
PROTEIN P53