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Endocrine and scavenging cell functions of a juvenile fish heart atrium: Fine structure aspects and translating conjectures

par Gilloteaux, Jacques;Jennes, Lothar;Vanderhaeghen, Jean-Jacques
Référence Translational Research in Anatomy, 32, 100252
Publication Publié, 2023-09

Article révisé par les pairs

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Résumé :

Background: The atrium of the juvenile teleost, smallmouth bass, Micropterus dolomieu Lacépède showed a pigmented endocardium. Our goal was to use fine structure to survey this fish heart tissues and verify the content responsible for this shrouding and discuss mammalian, translational conjectures about this cardiac structure. Methods: Using electron microscopy, heart pericardium, myocardium, and endocardium were analyzed, including atrial peptide immunolabeling. Results: The endocardium endothelial cells of the atrium revealed pinocytosis and endocytosis activities that resulted in accumulated electron-contrasted secondary lysosomes and lipofuscin bodies not found in the ventricle endocardium. This endothelium contacted subjacent atrial and ventricular myocardial cells producing immunolabeled atrial peptide-containing vesicles. Other migrating cells, including melano-macrophages, were noticed in the atrial sub endocardium. Conclusions: The endocardium functioned as a potent blood-heart barrier where transcytosis and dispatching of numerous materials, including those atrial peptides, between myocardium and the circulation occur. Peculiarly, this juvenile endothelium revealed abundant lysosomal processing of scavenged circulation materials like in a reticuloendothelial tissue. These juvenile cell's accumulated ‘aging’ lipofuscin bodies as organized deposits into a network with other organelles, especially mitochondria without evident disposal. Additionally, other cells, including melano-macrophages roamed both sub endocardium and ventricle; those also can influence the viewed pigmentation. Some of these data comforted the endocardial mesodermal lineage, still sketchy for all vertebrates while fish heart development is still used. These observations could raise questions: Does turnover of lipofuscin and associated captures make endocardial cells to model other mammalian pathologies, including those associated with heart failure?