Myocardial cell death in fibrillating and dilated human right atria

Journal of the American College of Cardiology

Volumn 34, Issue 5, 1999, Pages 1577-1586

  Aimé Sempé, Christine ^a   Folliguet, Thierry ^a   Rücker Martin, Catherine ^b   Krajewska, Maryla ^c   Krajewski, Stanislaw ^d   Heimburger, Michèle ^a   Aubier, Michel ^a   Mercadier, Jean Jacques ^b   Reed, John C ^c   Hatem, Stephane N ^d  

^a INSERM   (France)

^b CNRS   (France)

^c INSTITUT MUTUALISTE MONTSOURIS   (France)

^d BURNHAM INSTITUTE   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

CASPASE 3; KI 67 ANTIGEN;

ADULT; AGED; ANTIGEN EXPRESSION; APOPTOSIS; ARTICLE; CELL DEATH; CELL PROLIFERATION; CHROMATIN CONDENSATION; CLINICAL ARTICLE; CONTROLLED STUDY; FEMALE; HEART ATRIUM FIBRILLATION; HEART MUSCLE CELL; HISTOPATHOLOGY; HUMAN; HUMAN CELL; HUMAN TISSUE; MALE; PRIORITY JOURNAL; SARCOMERE;

EID: 0033231403     PISSN: 07351097     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0735-1097(99)00382-4     Document Type: Article

References (31)

1. The National Heart, Lung, and Blood Institute Working Group on Atrial Fibrillation. Atrial fibrillation: current understandings and research imperatives. J Am Coll Cardiol 1993;22:1830-4.
2. Moe GK. On the multiple wavelet hypothesis of atrial fibrillation. Arch Int Pharmacodyn Ther 1962;140:183-8.
3. Le Grand B, Hatem S, Deroubaix E, Couétil JP, Coraboeuf E. Depressed transient outward and calcium currents in dilated human atria. Cardiovasc Res 1994;28:548-56.
4. Allessie MA, Rensma PL, Brugada J, Smeets JLRM, Penn O, Kirchof CJHJ. Pathophysiology of atrial fibrillation. In: Zipes DP, Jalife J, editors. Cardiac Electrophysiology. From Cell to Bedside. Philadelphia: WB Saunders, 1990:59.
5. Fenoglio JJ, Duc Pham T, Hordof A, Edie RN, Wit AL. Right atrial ultrastructure in congenital heart disease. Atrial septal defects: effects of volume overload. Am J Cardiol 1979;43:820-7.
6. Mary-Rabine L, Albert A, Pham TD, Hordof A, et al. The relationship of human atrial cellular electrophysiology to clinical function and ultrastructure. Circ Res 1983;52:188-99.
7. Frustaci A, Chimenti C, Belloci F, Morgante E, Russo M, Maseri A. Histological substrate of atrial biopsies in patients with lone atrial fibrillation. Circulation 1997;96:1180-4.
8. Ausma J, Wijffels M, van Eys G, et al. Dedifferentiation of atrial cardiomyocytes as a result of chronic atrial fibrillation. Am J Pathol 1997;151:985-97.
9. Ausma J, Wijffels M, Thoné F, Wouters L, Allessie M, Borgers M. Structural changes of atrial myocardium due to sustained atrial fibrillation in the goat. Circulation 1997;96:3157-63.
10. Thornberry NA, Lazebnik Y. Caspases: enemies within. Science 1998;281:1312-6.
11. Tewari M, Quan LT, O'Rourke K, et al. Yama/CPP32b, a mammalian homolog of CED-3, is a CrmA-inhibitable protease that cleaves the death substrate poly (ADP-Ribose) polymerase. Cell. 1995;81:801-9.
12. Adams JM, Cory S. The Bcl-2 protein family: arbitrers of cell survival. Science 1998;281:1322-6.
13. Reed JC, Zha H, Aimé-Sempé C, Takayama S, Wang HV. Structure-function analysis of Bcl-2 family proteins. Regulators of programmed cell death. In: Gupta S, Cohen JJ, editors. Mechanisms of Lymphocytes Activation and Immune Regulation, Vol. VI. New York: Plenum Press, 1996:99-112.
14. Narula J, Haider N, Virmani R, et al. Apoptosis in myocytes in end-stage heart failure. N Engl J Med 1996;335:1182-9.
15. Mallat Z, Tedgui A, Fontaliran F, Frank R, Durigon M, Fontaine G. Evidence of apoptosis in arrhythmogenic right ventricular dysplasia. N Engl J Med 1996;335:1190-6.
16. Olivetti G, Abbi R, Quaini F, et al. Apoptosis in the failing human heart. N Engl J Med 1997;336:1131-41.
17. Misao J, Hayakawa Y, Ohno M, Kato S, Fujiwara T, Fujiwara H. Expression of Bcl-2 protein, an inhibitor of apoptosis, and Bax, an accelerator of apoptosis in ventricular myocytes of human hearts with myocardial infarction. Circulation 1996;94:1506-12.
18. Henry WL, Moranroth J, Pearlman AS, et al. Relation between echocardiographically determined left atrial size and atrial fibrillation. Circulation 1976;53:273-9.
19. Krajewska M, Wang HG, Krajewski S, et al. Immunohistochemical analysis of in vivo patterns of expression of CPP32 (Caspase-3), a cell death protease. Cancer Res 1997;57:1605-13.
20. Krajewski S, Krajewska M, Shabaik A, Miyashita T, Wang HG, Reed JC. Immunohistochemical determination of in vivo distribution of Bax, a dominant inhibitor of Bcl-2. Am J Pathol 1994;145:1323-36.
21. Nakopoulou L, Vourlaki C, Zervas A, Tzonou A, Gakiopoulou H, Dimopoulos MA. The prevalence of bcl-2, p53, and Ki-67 in transitional cell bladder carcinomas and their climcopathologic correlates. Hum Pathol 1998;129:146-54.
22. Benjamin EJ, Levy D, Vaziri S, Diagostino R, Belanger A, Wolf P. Independent risk factors for atrial fibrillation in a population-based cohort. JAMA 1994;271:840-4.
23. Mercadier JJ, De La Bastie D, Menasche P, et al. Alpha-myosin heavy chain isoform and atrial size in patients with various types of mitral valve dysfunction: a quantitative study. J Am Coll Cardiol 1987;9:1024-31.
24. Farzaneh F, Zalin R, Brill D, Shall S. DNA strand breaks and ADP-ribosyl transferase activation during cell differentiation. Nature 1982;300:362-6.
25. Johnstone AP, Williams GT. Role of DNA breaks and ADP-ribosyl transferase activity in eukaryotic differentiation demonstrated in human lymphocytes. Nature 1982;300:368-70.
26. Hanada M, Aimé-Sempé C, Sato T, Reed JC. Structure-function analysis of Bcl-2 protein. Identification of conserved domains important for homodimerization with Bcl-2 and heterodimerization with Bax. J Biol Chem 1995;270:11962-9.
27. Yin XM, Oltvai ZN, Korsmeyer SJ. BH1 and BH2 domains of bcl-2 are required for inhibition of apoptosis and heterodimerization with Bax. Nature 1994;369:321-33.
28. Cheng EHY, Kirsch DG, R.J. Clem RJ et al. Conversion of Bcl-2 to a Bax-like death effector by caspases. Science 1997;278:1966-8.
29. Hunter JJ, Bond BL, Parslow TG. Functional dissection of the human Bcl-2 protein: sequence requirements for inhibition of apoptosis. Mol Cell Biol 1996;16:877-83.
30. Stadelmann C, Brück W, Bancher C, Jellinger K, Lassmann H. Alzheimer disease: DNA fragmentation indicates increased neuronal vulnerability, but not apoptosis. J Neuropath Exp Neurology 1988;57:456-64.
31. Cheng W, Li B, Kajstura P, Li P, Wolin MS, Sonnenblick EH, Hintze TH, Olivetti G, Anversa P. Stretch-induced programmed myocyte cell death. J Clin Invest 1995;96:2247-59.