Prech, Marek and Marszalek, Andrzej and Schroeder, Josef and Filas, Violetta and Lesiak, Maciej and Jemielity, Marek and Araszkiewicz, Aleksander and Grajek, Stefan (2010) Apoptosis as a Mechanism for the Elimination of Cardiomyocytes After Acute Myocardial Infarction. AMERICAN JOURNAL OF CARDIOLOGY, 105 (9). pp. 1240-1245. ISSN 0002-9149,
Full text not available from this repository. (Request a copy)Abstract
Apoptosis is recognized as a mechanism of cell loss in the setting of acute myocardial infarction (AMI). Whether it contributes to myocyte elimination late after AMI has not yet been confirmed. We attempted to identify the features of apoptosis in myocytes that survived AMI. A search for ongoing apoptosis was performed in samples obtained from 38 human hearts: group I (n = 10), noncardiac death (control); and group II (n = 28), left ventricular aneurysm (in 20 patients, the samples were collected during aneurysmectomy and from 8 at autopsy). The morphometric evaluation included the degree of cellular hypertrophy, density of the capillary network, extent of myocytolysis, and features of apoptosis. Immunohistochemistry for caspase-3 and Bcl-2 was used as a prerequisite for transmission electron microscopy. Slides showing the strongest reaction for caspase-3 and negative for Bcl-2 were selected for transmission electron microscopy. CD-34 immunohistochemistry was used to quantify the capillary density. A significant reduction in capillary density was observed compared to the control group (1,085.6 +/- 205.0/mm(2) vs 2,968.7 +/- 457.3/mm(2); p < 0.001). Myocytes that survived the acute phase of AMI were significantly hypertrophied (24.5 +/- 4.7 mu m vs 14.5 +/- 1.6 mu m; p < 0.001) and showed a moderate to severe degree of myocytolysis. The average intensity score of the immunohistochemistry reactions for caspase-3 was 8.2 +/- 3.8. Using transmission electron microscopy, apoptotic bodies were found in caspase-3 positive samples. In conclusion, the expression of caspase-3 and the presence of apoptotic bodies confirmed apoptosis as a common pathway of cardiomyocyte death in the setting of a limited blood supply after AMI. (C) 2010 Elsevier Inc. All rights reserved. (Am J Cardiol 2010;105:1240-1245)
| Item Type: | Article |
|---|---|
| Uncontrolled Keywords: | HUMAN HIBERNATING MYOCARDIUM; ARTERY-OCCLUSION; HEART-FAILURE; CELL-DEATH; MYOCYTES; TISSUE; |
| Subjects: | 600 Technology > 610 Medical sciences Medicine |
| Divisions: | Medicine > Lehrstuhl für Pathologie |
| Depositing User: | Dr. Gernot Deinzer |
| Date Deposited: | 30 Jul 2020 12:55 |
| Last Modified: | 30 Jul 2020 12:55 |
| URI: | https://pred.uni-regensburg.de/id/eprint/24749 |
Actions (login required)
 |
View Item |
