Abstract
In studies of rat and human fetal livers, pinocytosis occurred on any part of the plasma membrane of early erythroblasts and it was not more frequent adjacent to a hepatic or Kupffer cell. This cell surface activity was observed both extravascularly and intravascularly. Formation of pinocytotic vesicles was more than just the internalization of parts of the plasma membrane of early erythroblasts. There was more electron scattering at the site where pinocytosis was being induced. Laminae of the unit membrane condensed to form a single electron-opaque membrane. At higher magnifications, even shallow invaginations were composed of 3 layers: an external amorphous layer with ferritin and other granules adherent to the membrane, the condensed plasma membrane, and an internal layer of relatively electron-opaque granules—presumably ribonucleoprotein. The resulting vesicles, with ferritin molecules and plasma inside, were bounded by a three-layered wall. These studies were extended to bone marrow from patients with pernicious anemia after therapy, acquired hemolytic anemia, erythremic myelosis, and sickle cell anemia. Some erythroblasts had areas of pinocytotic activity involving reticulum cells which Policard and Bessis (1958) called rhopheocytosis, a term Sorenson (1960) used similarly for areas involving developing hepatic cells, but these situations are not essential for the incorporation of ferritin. During embryonic hemopoiesis and adult erythropoiesis under pathologic conditions, ferritin molecules were attached to selective binding sites. Pinocytotic activity decreased with the maturation of erythroblasts.