Trophoblast invasion and alteration of mesometrial arteries in the pregnant hamster: Light and electron microscopic observations

During gestation in the Syrian golden hamster, an extensive migration of trophoblast into the maternal uteroplacental arterial system takes place. The present light and electron microscopic study has focused on one facet of this phenomenon, namely the trophoblastic invasion and alteration of the mes...

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Veröffentlicht in:Placenta (Eastbourne) 1982-07, Vol.3 (3), p.219-242
1. Verfasser: Carpenter, Stanley J.
Format: Artikel
Sprache:eng
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Zusammenfassung:During gestation in the Syrian golden hamster, an extensive migration of trophoblast into the maternal uteroplacental arterial system takes place. The present light and electron microscopic study has focused on one facet of this phenomenon, namely the trophoblastic invasion and alteration of the mesometrial ‘vascular knot’ (a complex of anastamosing, small arterial channels carrying blood to the chorio-allantoic placenta). Beginning at about the 8th day of gestation, motile trophoblastic giant cells (TGC), originating from the primitive trophospongium (Träger), invade and migrate as a wave up the central maternal arteries of the decidua basalis. During the 12th and 13th days of gestation, they reach the mesometrium and successively settle in the lumina of the vascular knot arterial channels. Between this time and parturition (day 16) the arrested TGC sequentially remove and replace the arterial endothelium, breach the elastic lamina, and apparently destroy (by lytic activity) nearly all of the mural smooth muscle. Near term, the vascular knot arterial channels are composed almost entirely of TGC. The functional significance of these events, and, more generally, the phenomenon of trophoblastic invasion of maternal uterine arteries in mamalian species having haemochorial-type placentae, are still uncertain. These invasions may be requisite to adapting, structurally and physiologically, the maternal uterine arteries to support of the fetoplacental unit and/or to maintaining the immunologically privileged status of the latter.
ISSN:0143-4004
1532-3102
DOI:10.1016/S0143-4004(82)80001-5