Ageing-induced ultrastructural changes of mitochondria of pulmonary vein sleeve cells

Masoud, Said; McDonald, Fraser; Bootman, Martin and Rietdorf, Katja (2015). Ageing-induced ultrastructural changes of mitochondria of pulmonary vein sleeve cells. In: Heart and Cardiac Muscle Abstracts, article no. PC183.


Atrial fibrillation (AF) is the most common form of sustained cardiac arrhythmia, with age being a significant risk factor. Inside the pulmonary veins a sheath of cardiomyocytes called pulmonary vein sleeve cells (PVCs) can be found. PVCs can cause atrial fibrillation by generating spontaneous increases in the intracellular Ca2+ concentration and ectopic electrical activity. Ultrastructural changes during atrial fibrillation have been described in atrial cardiomyocytes. Besides an increase in the number of glycogen granules, the reported changes include a greater variability in the number and size of mitochondria. However, the published data are inconsistent; some studies reported an increase of mitochondrial number and size in AF models, whereas other studies reported a decrease. So far, no studies have been performed to investigate changes in the mitochondrial structure occurring in PVCs. Since age is a significant risk factor for the development of AF we expected that the ultrastructure and/or number of mitochondria in PVCs would change with age. Here, we describe the results of a comparative ultrastructural study of pulmonary vein sleeve cells, atrial and ventricular cardiomyocytes from 3 and 24 month-old mice.

PVCs were isolated from mouse lung slices after agarose-inflation of the lungs. Atrial and ventricular cardiomyocytes were prepared from wedge-shaped sections of mouse hearts. We counted the number, and measured the size, of mitochondria in 25

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