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Development of the Human Placenta - Research Paper Example

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This essay, Development of the Human Placenta, talks about pacenta which is a fetomaternal organ that serves as a connection between mother and the developing fetus. The primary function of which is to carry nourishment and remove the waste products from the fetus. …
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Development of the Human Placenta
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 Placenta is a fetomaternal organ that serves as a connection between mother and the developing fetus. The primary function of which is to carry nourishment and remove the waste products from the fetus. Placenta has two components a fetal part that develops from the chorionic sac (chorionic villi) and a maternal part that develops from the endometrium (decidua basalis). Development of placenta begins after the cleavage of zygote, which consists of repeated mitotic divisions and the ultimate formation of a blastocyst. Blastomeres are separated into two parts by the blastocystic cavity, namely the trophoblast and the inner cell mass also called as embryo blast. Implantation is the first step in the development of placenta. Approximately at 6th day after fertilization the blastocyst attaches to the endometrium and the process of implantation begins. Now the trophoblast layer of the blastocyst at the embryonic pole gets differentiated into two layers, an inner layer called cytotrophoblast and an outer layer called as syncytiotrophoblast. Syncytiotrophoblast is highly invasive and expands quickly adjacent to the embryoblast, it produces enzymes that erode the maternal tissue enabling the blastocyst to burrow into the endometrium. The endometrial cells undergo apoptosis that facilitates invasion. The process of implantation is completed by the end of second week and the blastocyst is superficially implanted in the endometrium. At about day 10 blood filled lacunae appear in the syncytiotrophoblast which ultimately fuse at day 12 to form the lacunar network, the primordia of intervillous spaces of placenta,synsytiotrophoblast erodes the endometrial capillaries and maternal blood flows into these capillaries(sinusoids) giving rise to the primordial utero placental circulation. The rapidly proliferating cells of cytotrophoblast produce cellular extension that grow into the synsytiotrophoblast giving rise to the primary chorionic villi, mesenchyme soon grows into these primary villi giving rise to secondary villi.The mesenchymal cells soon differentiate into capillaries and blood cells, the villi at this stage are termed as tertiary villi they soon become connected with embryonic heart through vessels that differentiate in the mesenchyme. Cytotrophoblastic cells of the chorionic villi form a cytotrophoblastic shell that surrounds and attaches the chorionic sac to the endometrium. Villi that attach to the maternal tissues through the cytotrophoblastic shell are termed as stem villi from which the branch villi project. The decidua basalis is divided into many cotyledons by the placental septa, formed by the primary chorionic villi during erosion of the decidua basalis by them. Each cotyledon consists of one stem villus that gives rise to many branch chorionic villi and it is through the walls of these branch villi that the actual exchange of materials between the blood of mother and fetus occurs. At 20 weeks of pregnancy complete external membrane is formed consisting of amnion, chorion and decidua. Both maternal and fetal parts of placenta play role in immunoregulation that helps to protect the fetus from immune attack by the mother as the fetal part of placenta consists of both maternal and paternal genes that is it is an allograft, still it is not rejected by the mother’s immune system because of several reasons; 1. Trophoblastic cells express on their surface class I antigens including HLA-G that are nonpolymorphic and play role in allograft protection. 2. Syncytiotrophoblast of chorionic villi do not express MHC antigens on their surface and thus do not evoke an immune response. 3. Endometrium secretes certain immunosuppressive molecules for e.g; PGE2, TGF B and IL-10. 4. Ligands present on the trophoblast induce apoptosis of activated maternal leukocytes. 5. Increased percentage of CD 8+ cells and decrease in ratio of CD4+/CD8+ cells was found in distant and regional lymphatic organs during pregnancy. 6. Embryonic and fetal cells are always separated from each other by a layer of cytrotrophoblast (inner layer of trophoblast which is mononuclear) and syncyctiotrophoblast (outer layer of trophoblast which is multinucleated). This separation helps the fetus from maternal immunologic attacks. Changes in gene expression during human trophoblast differentiation: Through several studies genes involved in placental differentiation have been defined. By using a subtraction cDNA library between undifferentiated and differentiating cytotrophoblast cells six novel genes were identified which induced syncytial products during differentiation. These products are hCGα, pregnancy-specific β1 glycoprotein, 3β-hydroxysteroid dehydrogenase, plasminogen activator inhibitor PAI type I. Some of the other genes expressed in placenta that increased during differentiation are Keratin 19, calrectiulin, heat shock protein HSP 27, serum and gluccocorticoid regulated kinase and adrenomedullin. Homebox genes are a diverse group of genes which play important role in the embryonic development. Three homebox genes HB24, GAX and MSX2 are expressed both in the embryo and placenta Protein hormones involved in the formation of placenta: Placenta synthesizes a number of different hormones which includes: 1: Steroid hormones: They are the best examples of placental hormones and includes Progestins and Estrogens. Progestins support endometrium which is necessary for the survival of fetus and suppress contractility in uterine smooth muscle whereas Estrogen stimulates the growth of myometrium and mammary gland development. 2. Protein hormones: Several protein hormones are synthesized in placenta and includes i: Chorionic gonadotropin: These hormones stimulates the gonads , the human hormone is called human chorionic gonadotropin hCG and it is produced by fetal trophoblast cells and prevents luteal regression by binding to lutenizing hormone receptor. hCG is the first hormone produced during pregnancy and serves as the signal for maternal recognition of pregnancy. ii: Human Placental lactogens (hPL): The major source of hPL is villous synctiotrophoblasts. They regulate fetal and maternal metabolism and provides energy substrates for fetal use. iii: Relaxin: It is a small hormone and and is found in maternal serum through out pregnancy. The major source of relaxin in humans is corpus luteum, it functions in the relaxation of pelvic ligaments at the end of pregnancy. iv: Prolactin: Human prolactin is found in high levels in maternal serum. It major function is to help in lactation. v: Calcitonin: Trophoblasts also secrete calcitonin and functions in calcium homeostasis. Functions of Human placenta: Some of the functions of placenta are Placental permeability and membrane diffusion conductance: The primary function of placenta is to to promote selective transport of nutrients between the mother and the fetus. In the early months of pregnancy permeability of molecules is low because placental membrane is thick at that time and also because the surface are of placenta is small therefore diffusion is extremely low during early pregnancy. By the end of pregnancy rate of diffusion increases as placental membrane becomes comparatively thin and the surface area of placenta increases significantly. Diffusion of Oxygen through the placental membrane: The oxygen present in maternal blood passes into fetal blood by means of simple diffusion which is driven by an oxygen pressure gradient. Near the end of pregnancy the mean partial pressure of oxygen PO2 is higher in maternal blood than in fetal blood as a result of which oxygen readily diffuses from maternal to fetal blood. Even the partial pressure of oxygen PO2 in fetal blood is low but, it can still transport same amount of oxygen to tissues because of the higher concentration of hemoglobin (fetal hemoglobin) in fetal blood which is approximately 50 times higher than in maternal blood. The oxygen carrying capacity of fetal hemoglobin is higher than the adult hemoglobin. Diffusion of Carbon dioxide through the placental membrane: Carbon dioxide is continuously formed in the fetal tissues in the same way as it is formed in maternal tissues and is excreted into the mother’s blood through placenta. The partial pressure of carbon dioxide PCO2 in fetal blood is slightly higher than maternal blood which is enough to allow the diffusion of CO2 into maternal circulation and is excreted out through expiration from mother’s lungs. Diffusion of food stuffs through the placental membrane: Glucose is the major energy product required by the fetus. In late pregnancy fetus uses almost as much glucose as the mother’s and to provide this much glucose the trophoblast cells facilitate the diffusion of glucose through the placental membrane. As fatty acids are highly soluble in cell membrane they also diffuse from the maternal blood into the fetal blood but slowly than glucose so that fetus utilizes glucose easily for nutrition. Apart from these ketone bodies and potassium, sodium and chloride ions also diffuses easily from maternal to fetal blood. Excretion of waste products through the placental membrane: Excretory waste products diffuse through the placental membrane in a similar way as CO2 and then excreted out of the body along with the excretory products of the mother. These waste products include urea, uric acid and creatinine. Level of urea in fetus is slightly greater than that in maternal blood because urea easily diffuses through the placental membrane whereas creatinine does not diffuse out as easily as urea therefore its level in fetus is considerably higher than that in mother’s blood. Work cited: 1) Harvey J. Kliman ,From trophoblast to human placenta, from the encyclopedia of reproduction, Yale university of school and medicine http://med.yale.edu/obgyn/kliman/placenta/articles/EOR_Placenta/Trophtoplacenta.html 2) David Menton ,The placenta, a selfless servant, Answers January-March 2007 http://www.answersingenesis.org/articles/am/v2/n1/placenta 3) Benirschke, Kurt, Peter Kaufmann, and Rebecca N. Baergen. 2006. Pathology of the human placenta. New York: Springer. 4) Kliman, Harvey J. 1994. "Trophoblast infiltration". Reproductive Medicine Review. 3 (02). 5) Kliman, Harvey J, Placental hormones, Developmental and perinatal physiology http://www.med.yale.edu/obgyn/kliman/placenta/articles/Plac%20Hormones.html 6) Hall, John E., and Arthur C. Guyton. 2011. Guyton and Hall textbook of medical physiology. Philadelphia, Pa: Saunders/Elsevier. 7) Kliman, H. J. n.d. The placenta revealed. http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=1887036. 8) Moore, Keith L., T. V. N. Persaud, and Mark G. Torchia. 2008. The developing human clinically oriented embryology. Philadelphia, PA: Saunders/Elsevier. http://www.mdconsult.com/public/book/view?title=Moore+&+Persaud:+The+Developing+Human. 9) D Rukavina, M Kapovic and A Radojcic, 35: 275 - 278 (1991), Immunoregulatory factors contributing to fetal allograft survival, The international journal of developmental biology http://www.ijdb.ehu.es/web/paper.php?doi=1814410 Read More
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