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The aim of this work was to address morphometric patterns of coronary artery (c.a.) development in the rat based on serial section analysis of hearts at different stages of prenatal development. Studies were performed on foetal hearts 15–21 days (ED) post-conception. Paraffin sections were stained with haematoxylin-eosin (H&E) and frozen sections were labelled with Griffonia simplicifolia I (GSI) lectin (endothelial cell marker). Coronary arteries’ luminal diameters were measured at different distances from the aortic roots and the main c.a. branch lengths were calculated from serial sections. All measured values were compared to heart length and to foetal stages. On ED15 precursors of c.a. were distinguished as tubes running on both sides of the outflow tract. Below the aortic valves the tubes had the largest diameter. Formation and development of c.a. proceeded by elongation of vascular tubes distally, ramification and formation of the media and the adventitia. During the prenatal period the c.a. length increased approximately 14-fold, while heart length increased about 4-fold, and crown-rump length about 2.5-fold. The lumen of the proximal part of c.a. increased 4-fold during ED18–21. An increase in c.a. length is the fastest compared to the heart growth, and crown-rump growth during the foetal life.
Background: Research on the development and topography of mouse coronary arteries has been conducted for many years. Patterns of the course of these vessels have been described in various mouse strains. Our research focused on hearts of MIZZ mice. Materials and methods: We visualised the coronary artery system by means of latex dye perfusion via the aorta. The injected latex did not reach the capillary vessel system. Results: The heart of MIZZ mice is supplied with blood by two main coronary arteries: the right and the left one. They deliver blood to the right and left part of the heart, respectively. The right coronary artery arises from the right sinus of the aorta and the left coronary artery from the left sinus. The interventricular septum is usually supplied by the septal artery, which is the main branch of the right coronary artery. All arteries of the coronary system run intramurally. The number of branches and the location of their ostia differed among the examined individuals. Conclusions: Detailed information about the normal topography of coronary arteries, the number and course of their branches, as well as the area of the heart which is vascularised by these vessels constitutes the basic knowledge necessary to conduct further experiments. (Folia Morphol 2020; 79, 2: 255–264)
Cellular retinoic acid binding proteins are considered to be involved in retinoic acid (RA) signaling pathways. Our aim was to compare the expression and localization of cellular retinoic acid binding proteins I and II (CRABP I and II) in embryonic mouse hearts during normal development and after a single teratogenic dose of RA. Techniques such as real-time PCR, RT-PCR, Western blots and immunostaining were employed to examine hearts from embryos at 9-17 dpc. RA treatment at 8.5dpc affects production of CRABP I and II in the heart in the 48-h period. Changes in expression of mRNA for retinaldehyde dehydrogenase II (Raldh2), Crabp1 and Crabp2 genes also occur within the same time window (i.e. 10-11dpc) after RA treatment. In the embryonic control heart these proteins are localized in groups of cells within the outflow tract (OT), and the atrioventricular endocardial cushions. A gradient of labeling is observed with CRABP II but not for CRABP I along the myocardium of the looped heart at 11 dpc; this gradient is abolished in hearts treated with RA, whereas an increase of RALDH2 staining has been observed at 10 dpc in RA-treated hearts. Some populations of endocardial endothelial cells were intensively stained with anti-CRABP II whereas CRABP I was negative in these structures. These results suggest that CRABP I and II are independently regulated during heart development, playing different roles in RA signaling, essential for early remodeling of the heart tube and alignment of the great arteries to their respective ventricles.
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