L placentation as described here, and not just maintaining progesterone production
L placentation as described here, and not just maintaining progesterone 4-Deoxyuridine biological activity production by the corpus luteum for 3-4 weeks. It is well established that hyperglycosylated hCG drives invasion and implantation by placental trophoblastic cell deep into the myometrium of the uterus [13-16]. Hyperglycosylated hCG drives cytotrophoblast cell growth [8,13,14,16,17], and hCG promotes the fusion and differentiation of peripheral cytotrophoblast cells, where the blood supply is, to syncytiotrophoblast cells [17,18]. Hyperglycosylated hCG and hCG lead the implantation of placenta tissue into the uterus and the formation of villous trophoblast tissue. As illustrated in Figure 2 panel A, implanted blastocysts form columns of cytotrophoblast cells. Columns extend under the influence of hyperglycosylated hCG. As illustrated in panels B and C, hCG promotes differentiation of peripheral cells to active syncytiotrophoblast cells, closest to the circulation. Shape of syncytiotrophoblast cells forces arm formation and folding in developing villi (Figure 2 panels C and D). Taken together this generates villous trophoblastic tissue (panel D). While hCG and hyperglycosylated hCG force villous trophoblast tissue formation, hCG promotes the development and growth of uterine spiral arteries [19-26]. Angiogenesis forces the protrusion of arteries to reach invading villous trophoblast tissue [19-26]. hCG also promotes the formation of the umbilical circulation in villous tissue PubMed ID:http://www.ncbi.nlm.nih.gov/pubmed/27797473 and the formation of the umbilical cord [27-32]. While there is no clear evidence of how placental villi, the maternal uterine spiral arteries and fetal umbilical circulation are tied together to activate hemochorial placentation, all the component of hemochorial placentation are clearly hCG and hyperglycosylated hCG controlled. Figure 3 shows a human placenta and active hemochorial placentation. Histology shows that hemochorial placentation only becomes active by 10 weeks gestation. As illustrated in Figure 3, maternal blood fills the decidua parietalis chambers. Nutrients are passaged accross syncytiotrophoblast cells and into placental villi and into the developed fetal PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/28388412 umbilical circulation. Hyperglycosylated hCG functions in implantation are proven [13-16]. That hyperglycosylated hCG drives cytotrophoblast growth is shown and confirmed [8,13,14,16,17]. That hCG promotes the fusion of peripheral cytotrophoblast cells to syncytiotrophoblast cells is also proven [18]. That hCG drive uterine artery angiogenesis is demonstrated and confirmed multiple timesFigure 2 Formation of villous trophoblast. A. Cytotrophoblast columns in early implanted embryo. B. Extension of columns and differentiation of peripheral cells. B. and C. Folding of extensions caused by shape of syncytiotrophoblast cells. C and D formation of trophoblastic villi. No vascular supply, spiral arteries or fetal vasculature is shown.Cole Reproductive Biology and Endocrinology 2012, 10:24 http://www.rbej.com/content/10/1/Page 4 ofFigure 3 Human placental hemochorial placentation. While hCG and hyperglycosylated hCG force villous trophoblast tissue formation [13-17], hCG promotes the development and growth of uterine spiral arteries [19-26]. Angiogenesis forces the protrusion of arteries to reach invading villous trophoblast tissue [19-26]. hCG also promotes the formation of the umbilical circulation in villous tissue and the formation of the umbilical cord [27-32]. All linked together, villous trophoblast tissue, maternal spiral arte.