NDLI: Progressively developed myocardial apoptotic cell death during late phase of reperfusion

Please wait, while we are loading the content...

Progressively developed myocardial apoptotic cell death during late phase of reperfusion

Content Provider	Springer Nature Link
Author	Zhao, Zhi Qing Velez, Daniel A. Wang, Ning Ping Hewan Lowe, Karlene O. Nakamura, Masari Guyton, Robert A. Vinten Johansen, Jakob
Copyright Year	2001
Abstract	Myocardial apoptosis is primarily triggered during reperfusion (R). The aim of this study was to test the hypothesis that R-induced apoptosis develops progressively during the late phase of R, and that R-induced apoptosis is associated with changes in expression of anti- and pro-apoptotic proteins and infiltrated inflammatory cells. Thirty-one dogs were subjected to 60 min of left anterior descending coronary occlusion followed by 6, 24, 48, and 72 h R, respectively. There was no group difference in collateral blood flow, measured by colored microspheres during ischemia. Necrotic cell death (TTC staining) was significantly increased during R, starting at 27 ± 2% at 6 h R and increasing to 41 ± 2%† at 24 h R. There was no further change at 48 (37 ± 3%†) and 72 (36 ± 6%†) h R, respectively. TUNEL positive cells (% total normal nuclei) in the peri-necrotic zone progressively increased from 6 (26 ± 2) to 24 (38 ± 1†), 48 (48 ± 3†) and 72 (59 ± 4†) h R, respectively. The number of detected TUNEL positive cells at these time points was consistent with an increased intensity of DNA ladders, identified by agarose gel electrophoresis. Compared with normal tissue, western blot analysis showed persistent reduction in expression of anti-apoptotic protein Bcl-2 from 6 (16 ± 0.8%) to 72 h R (78 ± 2%†), and increase in expression of pro-apoptotic proteins including Bax from 6 (30 ± 3%) to 72 h R (66 ± 3%†), and p53 from 6 (12 ± 1%) to 72 h R (91 ± 2%†), respectively. Immunohistochemical staining revealed that infiltrated neutrophils (mm2 myocardium) were significantly correlated with development of necrotic and apoptotic cell death from 6 to 24 h R, respectively (P < 0.05), while large macrophage infiltration seen during 48 to 72 h R were correlated with apoptotic cell death (P < 0.05). These results indicate that 1) necrosis peaked at 24 h R when apoptosis was still progressively developing during later R; 2) changes in Bcl-2 family and p53 proteins may participate in R-induced myocardial apoptosis; 3) inflammatory cells may play a role in triggering cell death during R. * P < 0.05 vs. normal nuclei and tissue; † P < 0.01 vs. 6 h R.
Starting Page	279
Ending Page	290
Page Count	12
File Format	PDF
ISSN	13608185
Journal	Apoptosis
Volume Number	6
Issue Number	4
e-ISSN	1573675X
Language	English
Publisher	Kluwer Academic Publishers
Publisher Date	2001-01-01
Publisher Place	Boston
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Cancer Research Virology Anatomy Oncology Biochemistry
Content Type	Text
Resource Type	Article
Subject	Pharmaceutical Science Biochemistry (medical) Cell Biology Clinical Biochemistry Cancer Research Pharmacology

Sl.	Authority	Responsibilities	Communication Details
1	Ministry of Education (GoI), Department of Higher Education	Sanctioning Authority	https://www.education.gov.in/ict-initiatives
2	Indian Institute of Technology Kharagpur	Host Institute of the Project: The host institute of the project is responsible for providing infrastructure support and hosting the project	https://www.iitkgp.ac.in
3	National Digital Library of India Office, Indian Institute of Technology Kharagpur	The administrative and infrastructural headquarters of the project	Dr. B. Sutradhar bsutra@ndl.gov.in
4	Project PI / Joint PI	Principal Investigator and Joint Principal Investigators of the project	Dr. B. Sutradhar bsutra@ndl.gov.in Prof. Saswat Chakrabarti will be added soon
5	Website/Portal (Helpdesk)	Queries regarding NDLI and its services	support@ndl.gov.in
6	Contents and Copyright Issues	Queries related to content curation and copyright issues	content@ndl.gov.in
7	National Digital Library of India Club (NDLI Club)	Queries related to NDLI Club formation, support, user awareness program, seminar/symposium, collaboration, social media, promotion, and outreach	clubsupport@ndl.gov.in
8	Digital Preservation Centre (DPC)	Assistance with digitizing and archiving copyright-free printed books	dpc@ndl.gov.in
9	IDR Setup or Support	Queries related to establishment and support of Institutional Digital Repository (IDR) and IDR workshops	idr@ndl.gov.in

In vitro apoptotic cell death during erythroid differentiation

Apoptotic myocardial degeneration in thrombotic thrombocytopenic purpura

Protection of apoptotic cell death by protein A

Tissue transglutaminase mRNA expression in apoptotic cell death

Higenamine reduces apoptotic cell death by induction of heme oxygenase-1 in rat myocardial ischemia-reperfusion injury

Apoptotic action of estrogen

Homocysteine-thiolactone induces caspase-independent vascular endothelial cell death with apoptotic features

Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion

zVAD-fmk and DEVD-cho induced late mitosis arrest and apoptotic expressions

Progressively developed myocardial apoptotic cell death during late phase of reperfusion

Similar Documents

In vitro apoptotic cell death during erythroid differentiation

Apoptotic myocardial degeneration in thrombotic thrombocytopenic purpura

Protection of apoptotic cell death by protein A

Tissue transglutaminase mRNA expression in apoptotic cell death

Higenamine reduces apoptotic cell death by induction of heme oxygenase-1 in rat myocardial ischemia-reperfusion injury

Apoptotic action of estrogen

Homocysteine-thiolactone induces caspase-independent vascular endothelial cell death with apoptotic features

Role of insulin in the anti-apoptotic effect of glucose-insulin-potassium in rabbits with acute myocardial ischemia and reperfusion

zVAD-fmk and DEVD-cho induced late mitosis arrest and apoptotic expressions

Progressively developed myocardial apoptotic cell death during late phase of reperfusion