| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Cardiovascular Division, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, Massachuesetts 02215
Submitted 12 June 2003 ; accepted in final form 25 February 2004
Cardiac hypertrophy from pathological stimuli often proceeds to heart failure, whereas cardiac hypertrophy from physiological stimuli does not. In this study, physiological hypertrophy was created by a daily exercise regimen and pathological hypertrophy was created from a high-salt diet in Dahl salt-sensitive rats. The rats continued on a high-salt diet progressed to heart failure associated with an increased rate of terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling-positive cardiomyocytes. We analyzed primary cultures of these hearts and found that only cardiomyocytes made hypertrophic by a pathological stimulus show increased sensitivity to apoptosis. Examination of the molecular changes associated with these distinct types of hypertrophy revealed changes in Bcl-2 family members and caspases favoring survival during physiological hypertrophy. However, in pathological hypertrophy, there were more diffuse proapoptotic changes, including changes in Fas, the Bcl-2 protein family, and caspases. Therefore, we speculate that this increased sensitivity to apoptotic stimulation along with proapoptotic changes in the apoptosis program may contribute to the development of heart failure seen in pathological cardiac hypertrophy.
pathological; physiological; caspases; Bcl-2
This article has been cited by other articles:
|
|
 |
|
  S. C. Kolwicz, S. M. MacDonnell, B. F. Renna, P. O. Reger, R. Seqqat, K. Rafiq, Z. V. Kendrick, S. R. Houser, A. Sabri, and J. R. Libonati Left ventricular remodeling with exercise in hypertension Am J Physiol Heart Circ Physiol, October 1, 2009; 297(4): H1361 - H1368. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 L. Zelarayan, A. Renger, C. Noack, M.-P. Zafiriou, C. Gehrke, R. van der Nagel, R. Dietz, L. de Windt, and M. W. Bergmann NF-{kappa}B activation is required for adaptive cardiac hypertrophy Cardiovasc Res, August 27, 2009; (2009) cvp237v2. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. Choudhury, S. Bae, S. R. Kumar, Q. Ke, B. Yalamarti, J. H. Choi, L. A. Kirshenbaum, and P. M. Kang Role of AIF in cardiac apoptosis in hypertrophic cardiomyocytes from Dahl salt-sensitive rats Cardiovasc Res, August 14, 2009; (2009) cvp261v2. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y.-M. Sue, C.-F. Cheng, C.-C. Chang, Y. Chou, C.-H. Chen, and S.-H. Juan Antioxidation and anti-inflammation by haem oxygenase-1 contribute to protection by tetramethylpyrazine against gentamicin-induced apoptosis in murine renal tubular cells Nephrol. Dial. Transplant., March 1, 2009; 24(3): 769 - 777. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. J. Kriegel and A. S. Greene Substitution of Brown Norway chromosome 16 preserves cardiac function with aging in a salt-sensitive Dahl consomic rat Physiol Genomics, December 12, 2008; 36(1): 35 - 42. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
P. A. Watson, J. E. B. Reusch, S. A. McCune, L. A. Leinwand, S. W. Luckey, J. P. Konhilas, D. A. Brown, A. J. Chicco, G. C. Sparagna, C. S. Long, et al. Restoration of CREB function is linked to completion and stabilization of adaptive cardiac hypertrophy in response to exercise Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H246 - H259. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
N. Bodyak, D. L. Rigor, Y.-S. Chen, Y. Han, E. Bisping, W. T. Pu, and P. M. Kang Uncoupling protein 2 modulates cell viability in adult rat cardiomyocytes Am J Physiol Heart Circ Physiol, July 1, 2007; 293(1): H829 - H835. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 I. C. Okere, M. E. Young, T. A. McElfresh, D. J. Chess, V. G. Sharov, H. N. Sabbah, B. D. Hoit, P. Ernsberger, M. P. Chandler, and W. C. Stanley Low Carbohydrate/High-Fat Diet Attenuates Cardiac Hypertrophy, Remodeling, and Altered Gene Expression in Hypertension Hypertension, December 1, 2006; 48(6): 1116 - 1123. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 Y. Han, Y.-S. Chen, Z. Liu, N. Bodyak, D. Rigor, E. Bisping, W. T. Pu, and P. M. Kang Overexpression of HAX-1 Protects Cardiac Myocytes From Apoptosis Through Caspase-9 Inhibition Circ. Res., August 18, 2006; 99(4): 415 - 423. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
M. Marcil, K. Bourduas, A. Ascah, and Y. Burelle Exercise training induces respiratory substrate-specific decrease in Ca2+-induced permeability transition pore opening in heart mitochondria Am J Physiol Heart Circ Physiol, April 1, 2006; 290(4): H1549 - H1557. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. P. J. Buermans, E. M. Redout, A. E. Schiel, R. J. P. Musters, M. Zuidwijk, P. P. Eijk, C. van Hardeveld, S. Kasanmoentalib, F. C. Visser, B. Ylstra, et al. Microarray analysis reveals pivotal divergent mRNA expression profiles early in the development of either compensated ventricular hypertrophy or heart failure Physiol Genomics, May 11, 2005; 21(3): 314 - 323. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
S. W. Kong, N. Bodyak, P. Yue, Z. Liu, J. Brown, S. Izumo, and P. M. Kang Genetic expression profiles during physiological and pathological cardiac hypertrophy and heart failure in rats Physiol Genomics, March 21, 2005; 21(1): 34 - 42. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. B. Pillai, H. M. Russell, J. Raman, V. Jeevanandam, and M. P. Gupta Increased expression of poly(ADP-ribose) polymerase-1 contributes to caspase-independent myocyte cell death during heart failure Am J Physiol Heart Circ Physiol, February 1, 2005; 288(2): H486 - H496. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 B. C. Harrison, C. R. Roberts, D. B. Hood, M. Sweeney, J. M. Gould, E. W. Bush, and T. A. McKinsey The CRM1 Nuclear Export Receptor Controls Pathological Cardiac Gene Expression Mol. Cell. Biol., December 15, 2004; 24(24): 10636 - 10649. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| Visit Other APS Journals Online |
