Origin and fate of the central macrophages of erythroblastic islands in the fetal and neonatal mouse liver
- PMID: 9408906
- DOI: 10.1002/(SICI)1097-0029(19971201)39:5<398::AID-JEMT2>3.0.CO;2-D
Origin and fate of the central macrophages of erythroblastic islands in the fetal and neonatal mouse liver
Abstract
Erythroblastic islands were examined by ultrastructure and ultrastructural histochemistry in fetal and early neonatal livers of the mouse. The liver primordium of day 11 embryos contained not only immature hemopoietic cells in the hepatic cords but also macrophages in expanded sinusoids. At 12 and 13 days of gestation, macrophages bearing large cytoplasmic inclusions increased in number, and some of them moved from the sinusoids into the hepatic cords. A ring of erythroblasts surrounded the macrophages, and erythroblastic islands could be identified at 14 days of gestation. Fetal livers contained two kinds of macrophages: sinusoidal macrophages and central macrophages of the erythroblastic islands. These macrophages exhibited a similar binding pattern to Griffonia simplicifolia isoagglutinin-IB4 (GS-IB4) and soybean agglutinin (SBA). Fetal hepatocytes, however, did not appear to engage in active phagocytosis, and the binding patterns of GS-IB4 and SBA differed significantly between hepatocytes and the two kinds of macrophages. In the early postnatal mouse, a marked decrease in the number of erythroblastic islands occurred. Erythroblasts left the central macrophages, and the macrophages subsequently underwent degeneration. The erythroblastic islands finally disappeared at the end of liver hemopoiesis, and the degenerated central macrophages were removed by scavenger macrophages in the perisinusoidal space. Our data demonstrate that scavenger macrophages play an essential role in the development of hepatic hemopoiesis, with special reference to the formation and dissolution of erythroblastic islands.
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