The fusion of dorsal and ventral endocardial cushions in the embryonic chick heart: A study in fine structure

Abstract

Fusion of atrioventricular endocardial cushions begins during Hamburger‐Hamilton stage 27 and is completed during stage 28 (5 to 6 days incubation age). Connective tissue cells of these cushions are derived from the proliferating endocardial cell layer. The character of the organelles in cells of these cushions changes progressively as the cushions approach, meet and fuse: granular endoplasmic reticulum accumulates; Golgi complexes become extensive, and nuclei develop irregular shapes. These occur first in the connective tissue cells of the cardiac jelly and later in the endocardial cells. Fusion apparently is accomplished by liberation of the endocardial endothelial cells into the cardiac jelly, where, along with pre‐existing connective tissue cells, they become cells of the membranous interventricular septum. Gradually the cells appear to merge into one morphological population and thus become indistinguishable from each other. Both endocardial cells and connective tissue cells exhibit uptake of tritiated thymidine and undergo mitosis before, during and after fusion of the cushions. An outstanding characteristic of these cells is their continuing vitality throughout the entire process of fusion.

Diastolic Filling Characteristics in the Stage 12 to 27 Chick Embryo Ventricle

“…1). At these stages of development, the atrioventricular orifice is undivided and demarcated by the anterior and posterior endocardia1 cushions (6).…”

Fibulin-1, vitronectin, and fibronectin expression during avian cardiac valve and septa development

“…Alternatively, the immunolabeling patterns may be a reflection of cushion cell proliferation. Proliferation of the cushion cells is likely to be important in expansion and fusion of the cushions (Hay and Low, 1972;Markwald et al, 1977). If the newly produced cushion cells in the more densely packed and most mitotically active region proximal to the endocardium are secreting very little fibulin-1 or vitronectin at this stage, the observed distribution could be produced.…”

How to Make a Heart Valve: From Embryonic Development to Bioengineering of Living Valve Substitutes

“…The mechanism(s) by which the EC fuse remain largely unknown (Hay and Low 1972). However, aberrant fusion events cause membranous ventricular septal defects and extrafusion of the AoV cusps leads to BAV.…”