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Is apoptosis present in progression to chronic hypertensive heart failure?
1South Dakota Health Research Foundation-Cardiovascular Research Institute, Sioux Falls 57105-1570, USA.
Insights
Cardiomyocyte apoptosis is not a significant factor in hypertension-induced heart failure in spontaneously hypertensive heart failure (SHHF) rats. Further research should focus on myocyte nuclear structure for apoptosis studies.
Area of Science:
- Cardiovascular Research
- Cell Biology
- Pathology
Background:
- Hypertension is often associated with cardiomyocyte apoptosis.
- However, studies on spontaneously hypertensive heart failure (SHHF) rats suggest minimal myocyte loss.
- This discrepancy necessitates further investigation into myocyte apoptosis in this model.
Purpose of the Study:
- To investigate the role of cardiomyocyte apoptosis in myocardial remodeling in spontaneously hypertensive heart failure (SHHF) rats.
- To determine if myocyte loss occurs during hypertrophy and end-stage heart failure in SHHF rats.
Main Methods:
- In situ terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine 5'-triphosphate nick end-labeling (TUNEL) assay on heart sections from SHHF rats and Sprague-Dawley (SD) rats.
- Histological examination of optimally fixed heart tissues for myocyte damage or loss.
- Positive control with DNase treatment for TUNEL assay.
Main Results:
- No significant differences in TUNEL-positive cells were observed between SD, failing SHHF, and nonfailing SHHF rats.
- Extensive screening of optimally fixed failing hearts showed minimal evidence of myocyte loss.
- Nuclear characteristics suggestive of apoptosis were rarely found in failing SHHF rat myocytes.
Conclusions:
- Cardiomyocyte apoptosis does not appear to be a major mechanism in myocardial remodeling in SHHF rats.
- High-resolution microscopy of optimally fixed tissues is a recommended alternative for studying myocyte apoptosis.
Background:
Cardiomyocyte apoptosis is believed to occur in hypertension. Isolated myocyte data from spontaneously hypertensive heart failure (SHHF) rats, however, suggest that significant myocyte loss does not occur in this model. To investigate this issue further, heart sections from failing and nonfailing SHHF rats were examined by using in situ terminal deoxynucleotidyltransferase-mediated 2'-deoxyuridine 5'-triphosphate nick end-labeling (TUNEL). Additional hearts were optimally fixed by perfusion with glutaraldehyde and histologically examined for evidence of myocyte damage or loss.
Methods And Results:
Five Sprague-Dawley (SD) rats, 8 failing SHHF rats, and 6 nonfailing SHHF rats were perfusion-fixed with formaldehyde and used for TUNEL assay. Heart sections from each group were also treated with DNase for positive controls. There were no significant differences in the number of TUNEL-positive cells in SD, failing SHHF, and nonfailing SHHF rats. Additionally, extensive screening of 1-microm sections of optimally fixed failing hearts revealed little evidence of myocyte loss or nuclear characteristics suggestive of apoptosis.
Conclusion:
Apoptosis does not appear to be an important component of myocardial remodeling in SHHF rats during hypertrophy or end-stage heart failure. Examination of myocyte nuclear structure by high-resolution microscopy of optimally fixed tissues is recommended as an alternative approach to study apoptosis.