Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells

This study was designed to examine the autophagy in sino-atrial (SA) nodal cells from the normal adult mouse heart. Autophagy is the cellular process responsible for the degradation and recycling of long-lived and/or damaged cytoplasmic components by lysosomal digestion. In the heart, autophagy is k...

Full description

Bibliographic Details
Main Authors: Omatsu-Kanbe, Mariko, Yamamoto, Takefumi, Matsuura, Hiroshi
Format: Online
Language:English
Published: Japan Society of Histochemistry and Cytochemistry 2011
Online Access:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210427/
id pubmed-3210427
recordtype oai_dc
spelling pubmed-32104272011-11-17 Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells Omatsu-Kanbe, Mariko Yamamoto, Takefumi Matsuura, Hiroshi Regular Article This study was designed to examine the autophagy in sino-atrial (SA) nodal cells from the normal adult mouse heart. Autophagy is the cellular process responsible for the degradation and recycling of long-lived and/or damaged cytoplasmic components by lysosomal digestion. In the heart, autophagy is known to occur at a low level under physiological conditions, but to become upregulated when cells are exposed to certain stresses, such as ischemia. We examined whether the basal level of autophagy in SA nodal cells was different from that in ventricular or atrial myocytes. An ultrastructural analysis revealed that the SA nodal cells contained a number of autophagic vacuoles (autophagosomes) with various stages of degradation by lysosomal digestion, whereas the number of those in ventricular or 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 membrane protein 1 (LAMP1) indicated that the content of both autophagosomes and lysosomes were much greater in SA nodal cells than in ordinary cardiomyocytes. Our results provide evidence that the autophagy is active in normal SA nodal cells, which is not a stress-activated process but a constitutive event in the mouse heart. Japan Society of Histochemistry and Cytochemistry 2011-10-26 2011-08-10 /pmc/articles/PMC3210427/ /pubmed/22096262 http://dx.doi.org/10.1267/ahc.11030 Text en © 2011 The Japan Society of Histochemistry and Cytochemistry This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
repository_type Open Access Journal
institution_category Foreign Institution
institution US National Center for Biotechnology Information
building NCBI PubMed
collection Online Access
language English
format Online
author Omatsu-Kanbe, Mariko
Yamamoto, Takefumi
Matsuura, Hiroshi
spellingShingle Omatsu-Kanbe, Mariko
Yamamoto, Takefumi
Matsuura, Hiroshi
Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
author_facet Omatsu-Kanbe, Mariko
Yamamoto, Takefumi
Matsuura, Hiroshi
author_sort Omatsu-Kanbe, Mariko
title Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
title_short Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
title_full Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
title_fullStr Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
title_full_unstemmed Autophagy Is Constitutively Active in Normal Mouse Sino-Atrial Nodal Cells
title_sort autophagy is constitutively active in normal mouse sino-atrial nodal cells
description This study was designed to examine the autophagy in sino-atrial (SA) nodal cells from the normal adult mouse heart. Autophagy is the cellular process responsible for the degradation and recycling of long-lived and/or damaged cytoplasmic components by lysosomal digestion. In the heart, autophagy is known to occur at a low level under physiological conditions, but to become upregulated when cells are exposed to certain stresses, such as ischemia. We examined whether the basal level of autophagy in SA nodal cells was different from that in ventricular or atrial myocytes. An ultrastructural analysis revealed that the SA nodal cells contained a number of autophagic vacuoles (autophagosomes) with various stages of degradation by lysosomal digestion, whereas the number of those in ventricular or 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 membrane protein 1 (LAMP1) indicated that the content of both autophagosomes and lysosomes were much greater in SA nodal cells than in ordinary cardiomyocytes. Our results provide evidence that the autophagy is active in normal SA nodal cells, which is not a stress-activated process but a constitutive event in the mouse heart.
publisher Japan Society of Histochemistry and Cytochemistry
publishDate 2011
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3210427/
_version_ 1611485872248586240