Biological functions of hCG and hCG-related molecules.

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Abstract

hCG is a term referring to 4 independent molecules, each produced by separate cells and each having completely separate functions. These are hCG produced by villous syncytiotrophoblast cells, hyperglycosylated hCG produced by cytotrophoblast cells, free beta-subunit made by multiple primary non-trophoblastic malignancies, and pituitary hCG made by the gonadotrope cells of the anterior pituitary.

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Placental oxidative stress: from miscarriage to preeclampsia.

Eric Jauniaux, Andrew G. Burton (2004)

To review the role of oxidative stress in two common placental-related disorders of pregnancy, miscarriage and preeclampsia. Review of published literature. Miscarriage and preeclampsia manifest at contrasting stages of pregnancy, yet both have their roots in deficient trophoblast invasion during early gestation. Early after implantation, endovascular trophoblast cells migrate down the lumens of spiral arteries, and are associated with their physiological conversion into flaccid conduits. Initially these cells occlude the arteries, limiting maternal blood flow into the placenta. The embryo therefore develops in a low oxygen environment, protecting differentiating cells from damaging free radicals. Once embryogenesis is complete, the maternal intervillous circulation becomes fully established, and intraplacental oxygen concentration rises threefold. Onset of the circulation is normally a progressive periphery-center phenomenon, and high levels of oxidative stress in the periphery may induce formation of the chorion laeve. If trophoblast invasion is severely impaired, plugging of the spiral arteries is incomplete, and onset of the maternal intervillous circulation is premature and widespread throughout the placenta. Syncytiotrophoblastic oxidative damage is extensive, and likely a major contributory factor to miscarriage. Between these two extremes will be found differing degrees of trophoblast invasion compatible with ongoing pregnancy but resulting in deficient conversion of the spiral arteries and an ischemia-reperfusion-type phenomenon. Placental perfusion will be impaired to a greater or lesser extent, generating commensurate placental oxidative stress that is a major contributory factor to preeclampsia. Miscarriage, missed miscarriage, and early- and late-onset preeclampsia represent a spectrum of disorders secondary to deficient trophoblast invasion.

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Placental-related diseases of pregnancy: Involvement of oxidative stress and implications in human evolution.

Eric Jauniaux, Lucilla Poston, Graham J. Burton (2015)

Miscarriage and pre-eclampsia are the most common disorders of human pregnancy. Both are placental-related and exceptional in other mammalian species. Ultrasound imaging has enabled events during early pregnancy to be visualized in vivo for the first time. As a result, a new understanding of the early materno-fetal relationship has emerged and, with it, new insight into the pathogenesis of these disorders. Unifying the two is the concept of placental oxidative stress, with associated necrosis and apoptosis of the trophoblastic epithelium of the placental villous tree. In normal pregnancies, the earliest stages of development take place in a low oxygen (O2) environment. This physiological hypoxia of the early gestational sac protects the developing fetus against the deleterious and teratogenic effects of O2 free radicals (OFRs). In miscarriage, development of the placento-decidual interface is severely impaired leading to early and widespread onset of maternal blood flow and major oxidative degeneration. This mechanism is common to all miscarriages, with the time at which it occurs in the first trimester depending on the aetiology. In contrast, in pre-eclampsia the trophoblastic invasion is sufficient to allow early pregnancy phases of placentation but too shallow for complete transformation of the arterial utero-placental circulation, predisposing to a repetitive ischaemia-reperfusion (I/R) phenomenon. We suggest that pre-eclampsia is a three-stage disorder with the primary pathology being an excessive or atypical maternal immune response. This would impair the placentation process leading to chronic oxidative stress in the placenta and finally to diffuse maternal endothelial cell dysfunction.

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The lutropin/choriogonadotropin receptor, a 2002 perspective.

Mario Ascoli, Francesca Fanelli, Deborah Segaloff (2002)

Reproduction cannot take place without the proper functioning of the lutropin/choriogonadotropin receptor (LHR). When the LHR does not work properly, ovulation does not occur in females and Leydig cells do not develop normally in the male. Also, because the LHR is essential for sustaining the elevated levels of progesterone needed to maintain pregnancy during the first trimester, disruptions in the functions of the LHR during pregnancy have catastrophic consequences. As such, a full understanding of the biology of the LHR is essential to the survival of our species. In this review we summarize our current knowledge of the structure, functions, and regulation of this important receptor.

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Author and article information

Journal

Journal ID (iso-abbrev): Reprod Biol Endocrinol

Title: Reproductive biology and endocrinology : RB&E

Publisher: Springer Science and Business Media LLC

ISSN (Electronic): 1477-7827

ISSN (Print): 1477-7827

Publication date (Electronic): Aug 24 2010

Volume: 8

Affiliations

[1 ] USA hCG Reference Service, University of New Mexico, Albuquerque, NM 87131, USA. larry@hcglab.com

Article

Publisher Item ID: 1477-7827-8-102

DOI: 10.1186/1477-7827-8-102

PMC ID: 2936313

PubMed ID: 20735820

SO-VID: 40749a1a-b5ff-449c-b805-e3be6916325c

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Biological functions of hCG and hCG-related molecules.

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Most cited references 147

Placental oxidative stress: from miscarriage to preeclampsia.

Placental-related diseases of pregnancy: Involvement of oxidative stress and implications in human evolution.

The lutropin/choriogonadotropin receptor, a 2002 perspective.

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