Apoptosis and proliferation of cardiomyocytes in heart failure of different etiologies

Citation
D. Petrovic et al., Apoptosis and proliferation of cardiomyocytes in heart failure of different etiologies, CARDIO PATH, 9(3), 2000, pp. 149-152
Citations number
15
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
CARDIOVASCULAR PATHOLOGY
ISSN journal
10548807 → ACNP
Volume
9
Issue
3
Year of publication
2000
Pages
149 - 152
Database
ISI
SICI code
1054-8807(200005/06)9:3<149:AAPOCI>2.0.ZU;2-A
Abstract
Apoptosis and proliferation of myocytes were studied in human heart failure (HF). Endomyocardial samples from the right ventricle of 38 patients with terminal HF were compared with 10 traffic accident victims without a histor y of cardiovascular disease. The TUNEL method was used for the detection of apoptosis, and immunohistochemical methods were used for the evaluation of p53, bcl-2, proliferation cell nuclear antigen (PCNA), and proliferation m arker MIB-1. Apoptosis of cardiomyocytes, which was not p53-dependent, was present in 0. 07% of myocytes in HF, whereas no apoptotic myocytes were found in the cont rol group (p < 0.01). An increased expression of bcl-2 was found in HF comp ared to controls (p < 0.01), yet bcl-2 failed to protect myocytes from apop tosis. Increased expression of proliferation markers was found in myocytes in HF compared to controls (PCNA labeling: 3.7% vs. 1.2%, p < 0.01;MIB-1 la beling: 0.1% vs. 0%, p< 0.01). Nevertheless, no mitotic figures in cardiomy ocytes were found in our specimens. The volume density of interstitium was 22% in HF vs. 10% in the control group (p < 0.01). In conclusion, apoptosis of cardiomyocytes and fibrosis play an important r ole in HF, whereas clinical importance and the rate of myocyte proliferatio n remain to be determined. Cardiovasc Pathol 2000;9:149-152 (C) 2000 by Els evier Science Inc.