Ultrastructural changes of the myocardium in the embryonic rat heart

Abstract

Background Ultrastuctural changes of the embryonic heart have been described, and quantitative studies have reported the changes of cellular organelles in late fetal and postnatal development. However, no specific data are available on the quantitative morphology of the individual segments and intersegmental junctions of the early embryonic heart, although these components must have different functions. Methods We measured the absolute volumes of glycogen, Golgi complex, myofibrils, mitochondria, and the surface areas of the rough endoplasmic reticulum and mitochondrial cristae in the different regions of the embryonic rat heart by using stereological tools. Results During embryonic development, the cardiac segments and intersegmental junctions increase their glycogen volume. The sinuatrial junction and primary fold show a more rapid increase than all the other cardiac regions, whereas the atrioventricular canal shows a high level of glycogen content throughout the period studied. The Golgi complex and rough endoplasmic reticulum show a conspicuous decrease from day 15 onward. The cellular content of myofibrils and mitochondria and the surface area of the mitochondrial cristae show a gradual increase from day 11 to day 17 of development, but full maturation apparently takes place in late fetal and early postnatal stages. At day 15 of development, the cellular volumes of myofibrils and mitochondria show a temporary decrease. Conclusions The glycogen content cannot be explained on the basis of metabolism alone. The storage of glycogen is hypothesized to serve mechanical cell stability and may also be related to a target mechanism for ingrowing nerves. Myofibrillar and mitochondrial contents of the myocytes indicate a relatively late differentiation of the venous pole of the heart. Uninterrupted maturation is only started at the time of septation. Anat Rec. 248:233‐241, 1997. © 1997 Wiley‐Liss, Inc.

Embryonic Development of Heart in Indian Buffalo (Bubalus bubalis)

“…The myocardium of atria was thin as compared to ventricles and was loosely arranged in various directions, namely, circular, longitudinal, and oblique. Similar findings have been reported by [ 31 ] in rat. The nucleus of myocyte was single, large oval, or spherical with one or two nucleoli ( Figure 8 ).…”

Distribution of fibronectin, type I collagen, type IV collagen, and laminin in the cardiac jelly of the mouse embryonic heart with retinoic acid‐induced complete transposition of the great arteries

“…Candidate genes thought to regulate pattern formation include various nuclear retinoic acid receptors and cellular retinol/retinoic acid binding proteins, homeobox-containing genes and fibroblast growth factors (FGFs) (Brockes, 1989;Osmond, 1991;Cohn, 1995;Ohuchi, 1995;Niederreither, 1996;Kastner, 1997). In the developing heart, regional variations in the myocardial basement membrane seem to reflect secretory differences in the adjacent myocardium, since regional phenotypic differences in the myocardium have been observed, such as in the development of myofibrils, expression of myosin or actin isoforms, and transcription of homeobox-containing genes (Manasek, 1970;Ruzicka and Schwartz, 1988;De Groot, 1989;Robert, 1989;Chan-Thomas, 1993;Knaapen, 1997). RA shows the pharmacological effects on early embryonic myocardial progenitor cells and affects cellular differentiation, myofibril formation, and morphogenesis during development (Osmond, 1991;Dickman and Smith, 1996).…”

COPII–Golgi protein interactions regulate COPII coat assembly and Golgi size

“…Compartment size is somehow coupled to cell growth such that it increases as cells grow and remains roughly constant in postmitotic cells. On the other hand, during mitosis or differentiation, or in response to stress, secretory compartments can undergo extensive up-or downregulation depending on cell type, developmental timing, or stress condition (Knaapen et al, 1997;Lee and Linstedt, 1999;Lu et al, 2001;Colanzi et al, 2003;Yu et al, 2003). Thus, homeostatic mechanisms that maintain a proper balance of membrane input and output at each compartment must be suffi ciently fl exible to allow extensive, rapid, and reversible changes.…”