Author/Editor		Cleutjens, Jack PM
Title		The role of apoptosis in myocardial infarction
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. 393-401
Language		eng
Abstract		In previous studies we demonstrated activation of compnents of the intracardiac renin-angiotensin-system (RAS), such as renin and angiotensin I converting enzyme (ACE) following myocardial infarction (MI), leading to incrased levels of intracardiac angiotensin II (AngII), which stimulates DNA and collagen synthesis. In addition, the angiotensin II type 1 receptor (AT1) as well as the angiotensin II type 2 receptor (AT2) have been shown to be upregulated following MI. This activation of the intracardiac RAS following MI and the potential role of both AT receptors in AngII-induced apoptosis in vitro, makes Ang II a candidate for the trigger of apoptosis following MI in vivo. The objectives of this study were: determination of time dependent changes of the induction of apoptosis, determination of the phenotype of the apoptotic cells after MI and determination of the role of AT1 and AT2 receptors in the induction of apoptosis following MI. Apoptosis was transiently incrased after MI, but only in the infarcted left ventricle. The apoptotic index was significantly increased at 4 and 7 days after MI declining thereafter. Predominantly macrophages (22%) and endothelial cells (24%) and no myofibroblasts were phenotyped as apoptotic cells 1-90 days after MI. THe remaining 50-60% of the cells are most likely fibroblasts. No cardiomyocytes were determined as apoptotic cells, because the majority of apoptotic cardiomyocytes were determined earlier than 24 hours after MI. Both AT1 and AT2 receptor antagonists prevented apoptosis after MI, which indicates that angiotensin II is involved in the induction of apoptosis after MI.
Descriptors		MYOCARDIAL INFARCTION APOPTOSIS RECEPTORS, ANGIOTENSIN PEPTIDYL-DIPEPTIDASE A DNA NUCLEOTIDYLEXOTRANSFERASE ANGIOTENSIN-CONVERTING ENZYME INHIBITORS