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The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones

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The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones Placenlal Function and Fetal Nutrition, edited by Frederick C. Battaglia, Nestle Nutrition Workshop Series. Vol. 39. Nestec Ltd.. Vevey/Lippincott-Raven Publishers. Philadelphia. © 1997. The Endocrine Function of the Placenta: Interactions Between Trophic Peptides and Hormones Lise Cedard U. 361 INSERM, Maternite Baudelocque, 121 Boulevard de Port-Royal Paris, France The placenta is classically considered to be a source of hormones that play an important role in the establishment and maintenance of pregnancy. Because of its hemochorial structure, the human placenta produces hormones and easily secretes them into the maternal circulation. They include steroid hormones, such as estrogens and progesterone, and protein hormones, the most important of which are the chori- onic gonadotrophins (hCG), discovered in 1927. During the period from 1960 to 1980, the concept of a fetoplacental unit (1) with a complementary role for the fetus in steroid production offered a new approach to steroid metabolism, and since then new proteins and neuropeptides have been discovered (2,3). However, the lack of innervation of placental tissue highlights the importance of understanding neuroen- docrine regulation of placental physiology. Sophisticated culture methods enabling the study of biologic phenomena occurring during transformation of cytotrophoblast cells into a syncytiotrophoblast (4) have been combined with electron microscopy and histochemistry. Possibilities offered by molecular biology, including in situ hybridization and molecular cloning studies, have also completely modified current knowledge and revealed the presence of a multitude of factors, such as neuropeptides, cytokines, and growth factors, with their own receptors, but the role of these factors is often unclear. Results from these different approaches have recently added a new concept to the classic notion of endocrine production (with hormone secretion into the fetal or maternal circulation, followed by an eventual effect on other or- gans)—that of paracrine (between cells)/autocrine (into the same cell) regulation, varying at different stages of gestation and under pathologic conditions. STEROID HORMONES (2,5) Progesterone Progesterone clearly plays an important role in enabling implantation. It is neces- sary for the maintenance of a quiescent myometrium, which is impregnated with 59 60 TROPHIC PEPTIDE AND HORMONE INTERACTIONS this steroid through a process of diffusion from the site of placental insertion. It plays an important role in the development of the mammary gland and exerts a suppressive effect on lymphocyte proliferation and activity. Progesterone is produced by the corpus luteum in early pregnancy, with the relayed production by the placenta (the luteoplacental shift) occurring in the human from day 50 of pregnancy, then increasing in parallel with trophoblast growth (Fig. 1). At the end of pregnancy, the daily production is about 250 mg/d, with maternal blood levels of progesterone reaching 200 ng/mL. Progesterone cannot be synthesized by the trophoblast from acetate, but is derived from maternal cholesterol bound to low-density lipoproteins (LDL) (6) (Fig. 2). The uptake of LDL is accomplished by specific receptors present in the placental microvilli as early as the sixth week of pregnancy. Receptor-mediated endocytosis of LDL is followed by degradation of LDL in lysosomes (7). The pres- ence of scavenger receptors for acetyl-LDL and of specific binding sites for HDL3 increases the possibility of intemalization of the huge amount of cholesterol needed for both placenta development and progesterone biosynthesis (8). The placental production of progesterone was formerly considered as autonomous. In fact, its g IU/ml ug/ml 800 -| 40 -, r 8 600 - 30- - 6 400- 20- - 4 200- 10- - 2 o -i oJr I- 0 8 12 16 20 24 28 32 36 40 Weeks FIG. 1. Evolution of placental weight and levels of hPL and hCG during gestation. The level of hPL rises gradually until term in parallel with the placental growth. The circulating hCG level increases rapidly after implantation and reaches a peak at 8 to 12 weeks. After a drop, a plateau is observed until term. TROPHIC PEPTIDE AND HORMONE INTERACTIONS 61 1 eto-1'lacentai Unit Placenta Cholesterol j (C27) A 5-Pregnenolone| (C21) - A5, iP HSDH, A4"5 isomerase adrenal glands •"*" adrenal glands corticosterolds sulfatase sulfatase pHA| (C19) A-5, jp HSDH, A^-5 isomerase 17fi-HSDH A^-Androstenedione — •• Testosterone C19) aromatase enzymatic f complex X Estrone | ^ • |Estradiol-176 (C18) Liver 17fi-HSDH QH- MIA. $ FIG. 2. Biosynthesis of steroids in women from 10th week of pregnancy until labor. LDL, low- density lipoproteins. DHAS, dehydroepiandrosterone sulfate. regulation is extremely complex within the organ. The addition of a synthetic pre- cursor, 25-hydroxycholesterol, increases progesterone production in vitro by the presence of a specific cytochrome P450 (P450 sec). In the baboon, estrogens stimulate key steps in the progesterone biosynthetic pathway, namely LDL receptors and P450 sec (9), a process that in the human placenta in vitro is stimulated by hCG. The addition of pregnenolone to different placental preparations increases proges- terone production considerably, but the 3-hydroxydehydrogenase 5-4 isomerase (3- HSDH), which is not a rate-limiting factor by itself, can be inhibited by retroaction by 4-3 ketosteroids (androgens, progesterone) (10) and by estrogens. Catecholamines were shown to stimulate progesterone production by the adenylate cyclase protein A system. Activation of adenylate cyclase could also mediate the stimulating effect of luteinizing hormone (LH), hCG, vasoactive intestinal polypeptide (VIP), and prostaglandin E (11). Insulin-like growth factors (IGF-1 and IGF-2) (12) and epider- mal growth factor (EGF) stimulate progesterone production in vitro by their effect on cytochrome P450 sec and 3/3-HSDH. Other growth factors, such as transforming growth factor (TGF), platelet-derived growth factor (PDGF), and fibroblast growth factor (FGF), also increase the synthetic capacity of the trophoblast, probably by their role in the regulation of cell growth and differentiation (13). Apart from low 6-hydroxylation, progesterone cannot be metabolized by the human placenta, and about 25% of the progesterone produced by the placenta is transformed by the fetus into corticosteroids and androgens (Fig. 2). 62 TROPHIC PEPTIDE AND HORMONE INTERACTIONS Estrogens Estrogens have an important role in implantation and mammary gland develop- ment; they induce vasodilation within the maternal uterine vascular bed and enhance uterine contractility by regulating several subcellular mechanisms. The placenta is the main source of estrogen production after the ninth week of pregnancy, but as the human placenta lacks some steroidogenic activity, it has been assumed that steroidogenesis results from the fetoplacental unit. Estrogen production depends on the adrenal gland of the mother or fetus to supply androgens, particularly dehydroepi- androsterone (DHA) sulfate, which is hydrolyzed by a placental sulfatase to produce free DHA. Oxidation by 3-HSDH then forms the 4-androstenedione before aromati- zation by cytochrome P450 aromatase to produce estrone and estradiol, which are interconvertible under the action of a placental 17-dehydrogenase (Fig. 2). The placenta synthesizes estriol from the 16-DHA sulfate formed in the fetal liver. This steroid circulates in the maternal compartment as a sulfo or glycuro conjugate, whereas in the maternal blood, plasma estradiol (E2) is mainly in the free form and bound to the sex-binding globulin. The increased E2-to-progesterone ratio in late gestation is mainly caused by the rise in estrogen production by the placenta, which is itself caused by the development of the fetal adrenal cortex and by the constant increase in placental aromatase activity. Estrogen production by the placenta depends on many factors, such as evolution of the trophoblastic mass and of its blood flow, as well as stimulation by several more or less specific factors (14). Sulfatase, which is the rate-limiting factor in the placental metabolism of the DHA sulfate, is retroin- hibited by estrogens and by some progestins. It was initially demonstrated by in vitro perfusion that hCG stimulates aromatase activity through the intermediary of an increase in cyclic AMP production; prostaglandins F2, E2, and mainly E] have the same action. Several clinical conditions occurring in human pregnancy result in subnormal placental estrogen production. For example, in fetal anencephaly there is a decrease in secretion of the fetal adrenal C19 steroids, whereas in intrauterine growth retardation, DHA sulfate metabolism is impaired (15). When there is placen- tal sulfatase deficiency, an X-linked error of metabolism, estrogen secretion is very low, but the fetus shows normal development until term, as is the case with the more recently discovered deficiency of placental aromatase. It is thus evident that there is a considerable excess of estrogen production in human pregnancy. POLYPEPTIDE HORMONES (2,3) Human Chorionic Gonadotrophins The placenta is the primary source of hCG in pregnant women. It is essential for maintenance of pregnancy through its actions to increase luteal progesterone production until the placenta is able to produce adequate amounts of progesterone. The family of glycoprotein hormones to which hCG belongs comprises LH, folli- TROPHIC PEPTIDE AND HORMONE INTERACTIONS 63 cle stimulating hormone (FSH), and thyroid stimulating hormone
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