CG is produced by the trophoblastic cells of the placenta and stimulates the ovaries to synthesize the steroids that are essential for the maintenance of pregnancy.

[10] It is important to note here that the whole hCG protein hormone is a heterodimer, with an alpha and a beta subunit.

One likely reason for such high sequence similarity in hCG and LH is the fact that both respective beta subunits both bind to the same receptor, with their homology illustrating a common biological function and biochemical pathway.

[6] The very first nucleotide sequence of the gene encoding for the beta subunit of human chorionic gonadotropin (CGB) suggests that CGB evolved from a duplicate copy of the beta subunit of LH, another glycoprotein hormone with significant influence over pregnancy, expressed in the anterior pituitary gland.

These four genes share a 97-99% DNA sequence similarity, and code for the biochemically functional beta subunit of hCG.

CGB is the very first specific molecule synthesized by the embryo, with its RNA transcribed as early as the eight-cell stage.

CGB implements immunotolerance and angiogenesis at the endometrial maternal-fetal interface, which is particularly critical to the establishment of a successful pregnancy.

[15][16] As a more comprehensive overview: CGB promotes progesterone production by corpus luteal cells, promotes angiogenesis in uterine vasculature, promotes the fusion of cytotrophoblast cells and the subsequent differentiation to make syncytiotrophoblast cells, promotes the blockage of any immune or macrophage action by the maternal immune system on foreign invading placental cells, initiates proper and appropriate uterine growth parallel to fetal growth, suppresses any myometrial contractions during the course of pregnancy, stimulates growth and differentiation of the umbilical cord, prepares the endometrium for the approaching embryo implantation, acts on a receptor in mother's brain causing severe nausea and vomiting, and has also been shown to promote the growth of fetal organs during pregnancy.

Studies have indicated that patients who suffer from recurrent miscarriages possess an immunity dominated by what is called the Th1/Th2 hypothesis.

CGB encourages trophoblast invasion and interstitial theca cell proliferation through the overmodulation of extracellular-regulated kinase (ERK) and AKT signals, and the instigation of leptin production by CGB requires a dialogue between cAMP and p38 signaling pathways in the syncytiotrophoblast.

[15][16] The angiogenic effect of CGB on endothelial cells is precisely mediated through the activation of hCG/LH receptor and PKA/cAMP pathway.

It is through the binding of CGB to the hCG/LH receptor that the PKA/cAMP pathway is activated, which then helps stimulate angiogenesis and the establishment of a two-way nutrient highway for the embryo and subsequent fetus.

In tandem with CGB, the increased estrogen and progesterone signal to the body that pregnancy is occurring, and help thicken the uterine lining and stop menstruation.

[20][17] This article incorporates text from the United States National Library of Medicine, which is in the public domain.