Effects of aging and telomere length on inflammation and histological changes in the heart of wild house mouse

Abstract

Shortening of telomeres is known to be one of the main mechanisms behind cell death and biological aging of an organism. Moreover, short telomeres have found to associate with aging-related cardiovascular diseases (CVDs) and decreased immune defense. However, the causal role of short telomeres in the development of cardiovascular diseases and immunosenescence is still unclear.

The aim of this study was to clarify the causal role of telomere length and aging in development of CVD-related markers. Concentrations of mouse serum amyloid P (SAP) and prevalence of several opportunistic bacterial strains were measured to detect the changes in inflammatory response and immune system function. Moreover, stained paraffin sections of cardiac muscles of mice selected for divergent telomere lengths and age groups were studied to see the differences in cell size, capillary density and amount of collagen.

Aging increased cell size, number of capillaries per cell, amount of collagen and SAP concentrations. Telomere length did not affect the presence of CVD-related markers. However, the old mice with short telomeres had less collagen than the old long-telomere and control mice. Moreover, a positive correlation was found between relative telomere length of the old mice and collagen percentage, and in all mice between SAP concentration and collagen, and between the number of different bacterial strains and SAP concentration.

This study supports the idea that aging and immunosenescense expose to inflammation, and that risk of developing CVDs increases with advancing age. However, the results do not support the role of short telomeres in development of CVDs.