Characteristics of cardiac aging in C57BL/6 mice

Exp Gerontol. 2013 Mar;48(3):341-8. doi: 10.1016/j.exger.2013.01.005. Epub 2013 Jan 18.

Abstract

The specific processes that cause aging of the cardiac tissue remain elusive. C57BL/6 (B6) mice are commonly used for investigating age-related diseases in mammals. We thus sought to evaluate the cardiac aging process in B6 mice. Cardiac tissues from the newborn (B6 NB), 2month-old (B6 2M) and 21-27month-old B6 mice (B6 aged) were used for the investigation. Several age-related cellular processes were evaluated, including telomere shortening, changes in p53 and p16 expression, changes in mitochondria DNA expression and DNA deletion, and alteration of mitochondria. We found that the aging of the B6 mice cardiac tissue is associated with the maintenance of telomere length, increased expression of p53 and p16, mild changes in mitochondrial DNA expression but widespread DNA deletion, and significant alterations of the mitochondrial ultrastructure within the cardiac tissue. The results of our studies suggest that mitochondrial DNA deletions, which affect the mitochondrial ultrastructure, cytochrome C oxidase activity, and p53 expression, are significantly associated with cardiac aging and may be a source of age-related heart failure.

MeSH terms

  • Aging / genetics
  • Aging / metabolism*
  • Aging / pathology
  • Animals
  • Cyclin-Dependent Kinase Inhibitor p16 / metabolism
  • DNA, Mitochondrial / metabolism
  • Electron Transport Complex IV / metabolism
  • Gene Deletion
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Microscopy, Electron / methods
  • Mitochondria, Heart / metabolism
  • Mitochondria, Heart / ultrastructure
  • Myocardium / metabolism*
  • Myocardium / ultrastructure
  • Real-Time Polymerase Chain Reaction / methods
  • Telomere Homeostasis / physiology
  • Tumor Suppressor Protein p53 / metabolism

Substances

  • Cyclin-Dependent Kinase Inhibitor p16
  • DNA, Mitochondrial
  • Tumor Suppressor Protein p53
  • Electron Transport Complex IV