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Huppertz, B; Gauster, M; Orendi, K; König, J; Moser, G.
Oxygen as modulator of trophoblast invasion.
J Anat. 2009; 215(1): 14-20.
Doi: 10.1111/j.1469-7580.2008.01036.x
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- Führende Autor*innen der Med Uni Graz
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Huppertz Berthold
- Co-Autor*innen der Med Uni Graz
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Aubell Kristina
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Gauster Martin
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König Julia Maria
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Moser Gerit
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- Abstract:
- At the time of blastocyst implantation the uterine spiral arteries have already undergone morphological changes in the absence of any extravillous trophoblast invasion. Only 2 weeks after implantation, extravillous trophoblast cells develop and come into first contact with decidual tissues. Invading through the decidual interstitium, extravillous trophoblasts potentially reach and transform spiral arteries into uteroplacental arteries. Spiral arterial erosion starts at about mid-first trimester, whereas flow of maternal blood into the intervillous space is continuously established only at the beginning of the second trimester. One key regulator of the number of extravillous trophoblasts is oxygen. The steep gradient in oxygen concentration within the first trimester placenta is diminished with the onset of maternal blood flow. This gradient is used by the trophoblast to generate a large number of invasive cells to adapt the arterial vasculature in the placental bed to the growing needs of the fetus. Changes in oxygen concentrations or other factors leading to alterations in the rates of proliferation and/or apoptosis of extravillous trophoblast clearly impact on the remodelling of the vessels. The respective consequences of a failure in trophoblast invasion are growth restrictions of the baby and perhaps other pregnancy complications.
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Embryo Implantation - physiology
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Female -
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Fetal Growth Retardation - physiopathology
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Humans -
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Oxygen Consumption - physiology
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Pregnancy -
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Trophoblasts - physiology
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Uterine Artery - anatomy and histology
- Find related publications in this database (Keywords)
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extravillous trophoblast
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fetal growth restriction
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impaired invasion
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oxygen
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spiral artery