Chapter 14 - The Presence of LC3 and LAMP1 Is Greater in Normal Sino-Atrial Nodal Cells Than in Ordinary Cardiomyocytes, Indicating a Constitutive Event

Abstract

Autophagy is a widely conserved cellular process responsible for the lysosomal degradation and recycling of long-lived proteins and organelles. In the heart, autophagy stays at low levels under physiological conditions, but becomes activated when the myocardium is exposed to certain stresses, such as ischemia/reperfusion. The studies of autophagy in the heart have focused on the process in the ordinary cardiomyocytes, especially stressed ventricular myocytes, to elucidate whether it plays a beneficial or detrimental role in cardiac protection. Our studies on autophagy in normal adult mouse heart showed that the basal level of autophagy in sino-atrial (SA) nodal cells was higher than in ventricular or atrial myocytes. An electron microscopic analysis demonstrated that the SA nodal cells contained a number of autophagosomes with various stages of lysosomal degradation, while the number of autophagosomes in ordinary myocytes (ventricular and atrial myocytes) was either negligible or very small. The immunostaining of autophagosome marker microtubule-associated protein 1 light chain 3 (LC3) and lysosome marker lysosome-associated protein 1 (LAMP1) revealed that the presence of both autophagosomes and lysosomes is greater in SA nodal cells than in ordinary cardiomyocytes. Our results provide evidence that the high level of autophagy in normal SA nodal cells is not a stress-activated process but a constitutive event in the normal mouse heart.