| Regression of copper-deficient heart hypertrophy: reduction in the size of hypertrophic cardiomyocytes. | |
| | |
MedLine Citation:
|
PMID: 19027282 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
Dietary copper (Cu) deficiency causes cardiac hypertrophy and its transition to heart failure in a mouse model. Cu repletion results in rapid regression of cardiac hypertrophy and prevention of heart failure. The present study was undertaken to understand dynamic changes of cardiomyocytes in the hypertrophic heart during the regression. Dams of FVB mice were fed a Cu-deficient (CuD) diet (0.3 mg Cu/kg) starting on Day 3 post-delivery, and weanling pups were fed the same diet until Cu repletion (6.0 mg Cu/kg) in the diet at 31 days of age. Heart samples were obtained at the end of CuD feeding or at 3, 7, 14 or 28 days after Cu repletion. Cu deficiency resulted in increases in the size and reduction in the number of cardiomyocytes in the heart. Cu repletion led to regression in the size of hypertrophic cardiomyocytes and normalization of the total number of cardiomyocytes. Although a direct reduction in the cell size would be significantly responsible for the regression of heart hypertrophy, some hypertrophic cardiomyocytes upon Cu repletion reentered the cell cycle as determined by Ki-67 staining in the cardiomyocyte-specific alpha-sarcomeric actin-stained cells and underwent division as determined by a mitosis-specific marker, phospho-histone 3. Quantitative analysis indicated that the replication of hypertrophic cardiomyocytes made a contribution of about one-third to the total mitosis of the regenerated myocardium. This study suggests that a direct reduction in the size of some hypertrophic cardiomyocytes and a replication of other hypertrophic cardiomyocytes with reduced size make a significant contribution to the regression of CuD heart hypertrophy, leading to normalization of the size and the number of cardiomyocytes in the heart. |
| | |
Authors:
|
Zhanxiang Zhou; W Thomas Johnson; Y James Kang |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural Date: 2008-11-22 |
Journal Detail:
|
Title: The Journal of nutritional biochemistry Volume: 20 ISSN: 1873-4847 ISO Abbreviation: J. Nutr. Biochem. Publication Date: 2009 Aug |
Date Detail:
|
Created Date: 2009-07-14 Completed Date: 2009-08-13 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 9010081 Medline TA: J Nutr Biochem Country: United States |
Other Details:
|
Languages: eng Pagination: 621-8 Citation Subset: IM |
Affiliation:
|
Department of Medicine, University of Louisville School of Medicine, Louisville, KY 40202, USA. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Animals Cardiomegaly / diet therapy, pathology* Cell Count Cell Cycle Cell Size Copper / administration & dosage, deficiency* Disease Models, Animal Female Food, Formulated Heart / physiology Male Mice Mitochondria, Heart / pathology Mitosis Myocardium / pathology* Myocytes, Cardiac / pathology* Nutritional Status Regeneration* |
| Grant Support | |
ID/Acronym/Agency:
|
HL63760/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
|
7440-50-8/Copper |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Relation of sputum colour to bacterial load in acute exacerbations of COPD.
Next Document: The iron regulatory hormone hepcidin reduces ferroportin 1 content and iron release in H9C2 cardiomy...