Literature DB >> 12539576

Study on apoptosis and expression of P53, bcl-2, Bax in cardiac myocytys of congestive heart failure induced by ventricular pacing.

B Qi1, L Cao, L Wang, J Zhou.   

Abstract

The apoptosis and the expression of p53, bcl-2 and Bax in myocytes of chronic rapid ventricular pacing-induced congestive heart failure (CHF) in rabbits were investigated. The CHF rabbit model (P, n = 7) was established by chronic rapid ventricular pacing for 3 weeks. By using TUNEL technique the apoptosis in the myocytes in the rabbit model was studied and the expression of p53, bcl-2 and Bax in myocytes was detected by using immunohistochemical method. Sham-operated (C, n = 9) group served as control group. The results showed that there were about 4033 +/- 884.56 apoptotic cells/10(6) myocytes in P group, but no apoptotic cells were found in C group. Myocytes positive for p53 immunoreactivity (18.86 +/- 8.48 vs 5.06 +/- 0.87, P < 0.01) and positive for Bax immunoreactivity (7.15 +/- 1.91 vs 0.43 +/- 0.09, P < 0.01) were increased in P group as compared with those in C group, while the myocytes positive for bcl-2 immunoreactivity (7.08 +/- 1.05 vs 14.97 +/- 4.47, P < 0.01) and the ratio of bcl-2/Bax were decreased in P group as compared with those in C group. Apoptosis was involved in the development of CHF induced by continuously rapid ventricular pacing in rabbit. The expression of p53 and Bax was increased, while the expression of bcl-2 was inhibited. These might play an important role in the acceleration of the apoptosis.

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Year:  2001        PMID: 12539576     DOI: 10.1007/BF02886429

Source DB:  PubMed          Journal:  J Tongji Med Univ        ISSN: 0257-716X


  14 in total

1.  Apoptosis in the heart.

Authors:  W S Colucci
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Review 2.  Apoptosis in heart failure.

Authors:  H N Sabbah; V G Sharov
Journal:  Prog Cardiovasc Dis       Date:  1998 May-Jun       Impact factor: 8.194

3.  Bcl-2 targets the protein kinase Raf-1 to mitochondria.

Authors:  H G Wang; U R Rapp; J C Reed
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4.  Abnormalities of cardiocytes in regions bordering fibrous scars of dogs with heart failure.

Authors:  V G Sharov; H N Sabbah; A S Ali; H Shimoyama; M Lesch; S Goldstein
Journal:  Int J Cardiol       Date:  1997-08-08       Impact factor: 4.164

5.  Evidence of cardiocyte apoptosis in myocardium of dogs with chronic heart failure.

Authors:  V G Sharov; H N Sabbah; H Shimoyama; A V Goussev; M Lesch; S Goldstein
Journal:  Am J Pathol       Date:  1996-01       Impact factor: 4.307

6.  Bcl-2 heterodimerizes in vivo with a conserved homolog, Bax, that accelerates programmed cell death.

Authors:  Z N Oltvai; C L Milliman; S J Korsmeyer
Journal:  Cell       Date:  1993-08-27       Impact factor: 41.582

7.  Apoptosis in the failing human heart.

Authors:  G Olivetti; R Abbi; F Quaini; J Kajstura; W Cheng; J A Nitahara; E Quaini; C Di Loreto; C A Beltrami; S Krajewski; J C Reed; P Anversa
Journal:  N Engl J Med       Date:  1997-04-17       Impact factor: 91.245

8.  Abnormalities of contractile structures in viable myocytes of the failing heart.

Authors:  V G Sharov; H N Sabbah; H Shimoyama; A S Ali; T B Levine; M Lesch; S Goldstein
Journal:  Int J Cardiol       Date:  1994-03-01       Impact factor: 4.164

9.  Apoptosis in myocytes in end-stage heart failure.

Authors:  J Narula; N Haider; R Virmani; T G DiSalvo; F D Kolodgie; R J Hajjar; U Schmidt; M J Semigran; G W Dec; B A Khaw
Journal:  N Engl J Med       Date:  1996-10-17       Impact factor: 91.245

10.  Bad, a heterodimeric partner for Bcl-XL and Bcl-2, displaces Bax and promotes cell death.

Authors:  E Yang; J Zha; J Jockel; L H Boise; C B Thompson; S J Korsmeyer
Journal:  Cell       Date:  1995-01-27       Impact factor: 41.582

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