Abstract
Senescence of cardiac myocytes is frequently associated with heart diseases. To analyze senescence in cardiac myocytes, a number of biomarkers have been isolated. However, due to the complex nature of senescence, multiple markers are required for a single assay to accurately depict complex physiological changes associated with senescence. In single cells, changes in both cytoplasm and cell membrane during senescence can affect the changes in electrical impedance. Based on this phenomenon, we developed MEDoS, a novel microelectrochemical impedance spectroscopy for diagnosis of senescence, which allows us to precisely measure quantitative changes in electrical properties of aging cells. Using cardiac myocytes isolated from 3-, 6-, and 18-month-old isogenic zebrafish, we examined the efficacy of MEDoS and showed that MEDoS can identify discernible changes in electrical impedance. Taken together, our data demonstrated that electrical impedance in cells at different ages is distinct with quantitative values; these results were comparable with previously reported ones. Therefore, we propose that MEDoS be used as a new biomarker-independent methodology to obtain quantitative data on the biological senescence status of individual cells.
Highlights
Senescence and disease are the two main contributing factors for the termination of life [1]
We developed microelectrochemical impedance spectroscopy for diagnosis of senescence (MEDoS)
Changes in cell impedance during senescence in the three different age groups of zebrafish were evaluated in terms of magnitude and phase angle at the measured frequencies
Summary
Senescence and disease are the two main contributing factors for the termination of life [1]. Senescence is one of the major causative factors of disease, senescence can be controlled to extend lifespan. In this context, various biomarkers have been used to measure and analyze senescence. Senescent cells have reduced autophagic activity [3], reduced telomerase activity [4], altered contents in mitochondrial phospholipid [5], increased oxidative stress due to reactive oxygen species (ROS) [6, 7], and increased levels of senescence associated β-galactosidase activity [8]. In all of the aforementioned studies, specific biomarkers have been used to evaluate the potential alterations in cell structure and function. Such analyses involve complex procedures including chemical modification or tagging. Given that senescence is a highly complex biological process, it is difficult to assess cellular aging based on the limited number of available biomarkers
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