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  • Title: Altered trophoblastic differentiation and increased trophoblastic invasiveness during delayed development in the short-tailed fruit bat, Carollia perspicillata.
    Author: Badwaik NK, Rasweiler JJ.
    Journal: Placenta; 2001 Jan; 22(1):124-44. PubMed ID: 11162361.
    Abstract:
    During pregnancy in the short-tailed fruit bat, lengthy post-implantational delays in conceptus development can occur in response to stress in captivity and seasonally in the wild. When comparisons were made between uteri carrying embryos in delay at the primitive streak stage and those growing more rapidly, many differences were noted. During delay the developing chorioallantoic placenta was generally smaller, contained a higher ratio of cytotrophoblast to syncytiotrophoblast, and had been invaded only to a limited extent on its embryonic side by mesoderm. Furthermore, much of the cytotrophoblast appeared relatively undifferentiated, randomly-oriented, linked primarily by primitive junctions, and lacked a basal lamina. In contrast, in placentae serving somite and limb-bud stage embryos, sizeable areas were noted that consisted only of more highly differentiated syncytiotrophoblast perforated by maternal vascular spaces (trophospongium). The first contact of the allantois with the developing placenta was also noted at the somite stage, and this initiated widespread invasion of the placenta by mesenchyme and allantoic blood vessels. Wherever this invasion had occurred, the cytotrophoblast between the mesenchyme and syncytiotrophoblast of the interhaemal barrier consisted of a single, polarized layer of more differentiated cells with an associated basal lamina. Eventually, all of the trophospongium was invaded by cytotrophoblast and vascularized fetal mesenchyme. These observations suggest that in addition to its germinal function, cytotrophoblast in this bat may play a major role in controlling mesenchymal invasion and angiogenesis on the embryonic side of the placenta. During the period of delay, highly invasive trophoblast is also released by the placenta. This invades the myometrium and sometimes extrauterine tissues via interstitial migration along maternal capillaries and veins.
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