Placental Hormones
Placental Lactogen
Placenta
Chorionic Gonadotropin
Trophoblasts
Pregnancy
Hormones
Thyroid Hormones
Follicle Stimulating Hormone
Luteinizing Hormone
Parathyroid Hormone
Gonadotropin-Releasing Hormone
Basic homopolyamino acids, histones and protamines are potent antagonists of angiogenin binding to ribonuclease inhibitor. (1/83)
A radio-ribonuclease inhibitor assay based on the interaction of 125I-angiogenin with ribonuclease inhibitor (RI) was used to detect pancreatic-type ribonucleases and potential modulators of their action. We show that highly basic proteins including the homopolypeptides poly-arginine, poly-lysine and poly-ornithine, core histones, spermatid-specific S1 protein and the protamines HP3 and Z3 were strong inhibitors of angiogenin binding to RI. A minimum size of poly-arginine and poly-lysine was required for efficient inhibition. The inhibition likely resulted from direct association of the basic proteins with the acidic inhibitor, as RI bound to poly-lysine and protamines while 125I-angiogenin did not. Antagonists of the angiogenin-RI interaction are potential regulators of either angiogenin-triggered angiogenesis and/or intracellular RI function, depending on their preferential target. (+info)Induction of megakaryocyte differentiation by a novel pregnancy-specific hormone. (2/83)
Maturation of megakaryocytes and subsequent platelet release are normally regulated by a network of cytokines, including thrombopoietin and various interleukins. Because abnormal platelet production and activation have been implicated in gestational pathologies, additional pregnancy-specific cytokines may play important roles in the regulation of megakaryocytopoiesis. Consistent with this hypothesis, we have found that the hormone prolactin-like protein E, a placental hormone that we have recently characterized, targets megakaryocytes through a specific cell surface receptor and induces megakaryocyte differentiation through a gp130-dependent signal transduction pathway. (+info)Altered arterial concentrations of placental hormones during maximal placental growth in a model of placental insufficiency. (3/83)
Pregnant ewes were exposed chronically to thermoneutral (TN; 20+/-2 degrees C, 30% relative humidity; n=8) or hyperthermic (HT; 40+/-2 degrees C 12 h/day, 35+/-2 degrees C 12 h/day, 30% relative humidity, n=6) environments between days 37 and 93 of pregnancy. Ewes were killed following 56 days of exposure to either environment (days in treatment (dit)), corresponding to 93+/-1 day post coitus (dpc). Maternal core body temperatures (CBT) in HT ewes were significantly elevated above the TN ewes (HT; 39.86+/-0.1 degrees C vs TN; 39.20+/-0.1 degrees C; P<0.001). Both groups of animals displayed circadian CBT, though HT ewes had elevated amplitudes (HT; 0.181+/-0.002 degrees C vs TN; 0.091+/-0.002 degrees C; P<0.001) and increased phase shift constants (HT; 2100 h vs TN; 1800 h; P<0.001). Ewes exposed to chronic heat stress had significantly reduced progesterone and ovine placental lactogen (oPL) concentrations from 72 and 62 dpc respectively (P<0.05), corresponding to approximately 30 dit. However, when compared with the TN ewes, HT cotyledonary tissue oPL mRNA and protein concentrations were not significantly different (P>0.1). Prolactin concentrations rose immediately upon entry into the HT environment, reaching concentrations approximately four times that of TN ewes, a level maintained throughout the study (HT; 216.31+/-32.82 vs TN; 54. 40+/-10.0; P<0.0001). Despite similar feed intakes and euglycemia in both groups of ewes, HT fetal body weights were significantly reduced when compared with TN fetuses (HT; 514.6+/-48.7 vs TN; 703. 4+/-44.8; P<0.05), while placental weights (HT; 363.6+/-63.3 vs TN; 571.2+/-95.9) were not significantly affected by 56 days of heat exposure. Furthermore, the relationship between body weight and fetal length, the ponderal index, was significantly reduced in HT fetuses (HT; 3.01+/-0.13 vs TN; 3.57+/-0.18; P<0.05). HT fetal liver weights were also significantly reduced (HT; 27.31+/-4.73 vs TN; 45.16+/-6.16; P<0.05) and as a result, the brain/liver weight ratio was increased. This study demonstrates that chronic heat exposure lowers circulating placental hormone concentrations. The observation that PL mRNA and protein contents are similar across the two treatments, suggests that reduced hormone concentrations are the result of impaired trophoblast cell development, specifically trophoblast migration. Furthermore, the impact of heat exposure during maximal placental growth is great enough to restrict early fetal development, even before the fetal maximal growth phase (100 dpc-term). These data highlight that intrauterine growth retardation (IUGR) may result primarily from placental trophoblast cell dysfunction, and secondarily from later reduced placental size. (+info)Hormonal control of protein expression and mRNA levels of the MaxiK channel alpha subunit in myometrium. (4/83)
Large conductance voltage-dependent and Ca(2+)-modulated K(+) channels play a crucial role in myometrium contractility. Western blots and immunocytochemistry of rat uterine sections or isolated cells show that MaxiK channel protein signals drastically decrease towards the end of pregnancy. Consistent with a transcriptional regulation of channel expression, mRNA levels quantified with the ribonuclease protection assay correlated well with MaxiK protein levels. As a control, Na(+)/K(+)-ATPase protein and RNA levels do not significantly change at different stages of pregnancy. The low numbers of MaxiK channels at the end of pregnancy may facilitate uterine contraction needed for parturition. (+info)Effects of dopamine and melatonin on the regulation of the PIT-1 isotype, placental growth hormone and lactogen gene expressions in the rat placenta. (5/83)
Rat placenta produces several members of the placental prolactin-growth hormone (PRL-GH), including placental lactogen (PL) and placental prolactin like protein (PLP), during pregnancy. It is important to study placental local regulators that control the expression of PRL-GH genes. We have previously reported that dopamine (DA) can regulate Pit-1 and PL-II gene expressions. In this study we aimed to investigate the local expression of melatonin receptor 1a (Mel1a) and the effects of DA and melatonin on the expressions of PL-Iv, PL-II, PLP-C genes and Pit-1 gene that are involved in the expression of PRL-GH genes in the rat pituitary and placenta. According to the Northern blot analysis, DA receptor 2 (D2) was expressed in the rat placenta. We also report on the local expression of Mel1a in the rat placenta for the first time. Injected DA agonist, bromocriptine (in vivo) decreased PL-Iv, PLP-C and Pit-1 mRNA levels in the rat placenta. The melatonin agonist, chloromelatonin in culture media also decreased the levels of PL-Iv, PL-II and PLP-C mRNA. However, melatonin does not affect the Pit-1 mRNA level. These data suggest that D2 and Mel1a may control the expression of PRL-GH genes in the rat placenta and its response to the extracellular changes of DA and melatonin secreted from the maternal organ. However, Pit-1 may not be involved in the Mel1a induced inhibition of PRL-GH gene expressions in the rat placenta. (+info)Cytoplasmic sequestration and functional repression of p53 in the mammary epithelium is reversed by hormonal treatment. (6/83)
Proper function of the p53 tumor suppressor gene is critical for inhibiting tumor development in a broad spectrum of tissues. Although the mammary gland is highly susceptible to tumor formation, the functional status of p53 in the normal tissue had not been investigated. Therefore, expression, localization, and activity of p53 were examined in normal mammary tissues. High levels of p53 protein were found expressed in the cytoplasm of the ductal epithelium of the quiescent mammary gland. Ionizing radiation failed to recruit p53 to the nucleus, and p53-dependent responses were minimal. However, transient hormonal stimulation resulted in nuclear accumulation of p53, an induction of p21/WAF1, and a 5-fold increase in apoptosis after ionizing radiation. Therefore, the functional state of wild-type p53 in the mammary epithelium can be regulated by hormonal stimuli. (+info)A member of the nuclear factor-1 family is involved in the pituitary repression of the human placental growth hormone genes. (7/83)
The human growth hormone (GH) gene family consists of five tandemly arranged and highly related genes, including the chorionic somatomammotropins (CSs), at a single locus on chromosome 17. Despite striking homologies in promoter and flanking DNA sequences, the genes within this locus have different tissue-specific patterns of expression: GH-N is expressed almost exclusively in the somatotrophs of the anterior pituitary; the remaining genes, including CS-A, are expressed in placental syncytiotrophoblast. Previously we proposed that active repression of the placental gene promoters in pituitary GC cells is mediated by upstream 'P' sequences and, specifically, a 263 bp region containing two 'P' sequence elements (PSE-A and PSE-B) and corresponding factors (PSF-A and PSF-B). We have now examined the possibility that PSF-A and PSF-B are members of the nuclear factor (NF)-1 family. Transcripts of NF-1A, NF-1C and NF-1X, but not of NF-1B, were readily detected in GC cells. High-affinity binding of NF-1 to PSE-B, but not to PSE-A, was confirmed by competition of DNA-protein interactions by using NF-1 DNA elements and antibodies. Functionally, a NF-1 element was able to substitute for PSE-B as a promoter-specific repressor in GC cells after gene transfer. However, there was a difference in the magnitude of repression exerted by the NF-1 and PSF-B elements on the CS-A promoter and, with the use of mutations, this difference was shown to be consistent with variations in NF-1-binding sequences. These results indicate that PSF-B, but not PSF-A, is a member of the NF-1 family, which participates in the PSF complex and in the repression of the CS-A promoter in pituitary GC cells. (+info)Expression of insulin-like growth factor-I and placental growth hormone mRNA in placentae: a comparison between normal and intrauterine growth retardation pregnancies. (8/83)
Intrauterine growth restriction (IUGR) is generally defined as the pathological restriction of fetal growth resulting in a fetus with birth weight below the 10th percentile for gestational age. Almost 75% of IUGR cases develop during third trimester. Studies on animals (rodents and sheep) as well as humans suggest that insulin-like growth factor-I (IGF-I), under the influence of placental growth hormone (PGH) plays crucial roles in fetal growth regulation during this period. Limited data are available with regard to IGF-I and PGH in placentae of normal and IUGR births. Therefore, in the present study, IGF-I and PGH mRNA expression has been studied in term placentae of normal (n = 10) and IUGR (n = 15) births by in-situ hybridization procedure. Their expression was also studied in first (n = 5) and second (n = 5) trimester placentae obtained from elective termination of normal pregnancies. Both IGF-I and PGH expression were found to be higher in the first and second trimester placentae compared to term placentae in normal pregnancies. However, IUGR term placentae showed increased expression of both IGF-I and PGH mRNA in comparison with normal placentae. Various mechanisms leading to the increased transcription of IGF-I and PGH mRNA in IUGR placenta are discussed. This increased transcription perhaps occurs in response to the reduction in the fetal growth. (+info)Placental hormones are a type of hormones that are produced by the placenta, an organ that develops in the uterus during pregnancy. These hormones play a crucial role in maintaining and supporting a healthy pregnancy. Some of the key placental hormones include:
1. Human Chorionic Gonadotropin (hCG): This hormone is produced after implantation and is detected in the urine or blood to confirm pregnancy. It maintains the corpus luteum, which produces progesterone during early pregnancy.
2. Progesterone: This hormone is critical for preparing the uterus for pregnancy and maintaining the pregnancy. It suppresses maternal immune response to prevent rejection of the developing embryo/fetus.
3. Estrogen: This hormone plays a vital role in the growth and development of the fetal brain, as well as promoting the growth of the uterus and mammary glands during pregnancy.
4. Human Placental Lactogen (hPL): This hormone stimulates maternal metabolism to provide nutrients for the developing fetus and helps prepare the breasts for lactation.
5. Relaxin: This hormone relaxes the pelvic ligaments and softens and widens the cervix in preparation for childbirth.
These hormones work together to support fetal growth, maintain pregnancy, and prepare the mother's body for childbirth and lactation.
Placental lactogen is a hormone produced by the placenta during pregnancy in humans and some other mammals. It is similar in structure to human growth hormone and prolactin, and has both growth-promoting and lactogenic (milk-producing) properties. Placental lactogen plays an important role in regulating maternal metabolism during pregnancy, promoting the growth and development of the fetus, and preparing the mother's body for lactation after birth. It helps to stimulate the growth of the mammary glands and the production of milk by increasing the availability of nutrients such as glucose, amino acids, and fatty acids in the mother's bloodstream. Placental lactogen also helps to regulate the mother's insulin sensitivity, which can affect her energy levels and the growth of the fetus.
The placenta is an organ that develops in the uterus during pregnancy and provides oxygen and nutrients to the growing baby through the umbilical cord. It also removes waste products from the baby's blood. The placenta attaches to the wall of the uterus, and the baby's side of the placenta contains many tiny blood vessels that connect to the baby's circulatory system. This allows for the exchange of oxygen, nutrients, and waste between the mother's and baby's blood. After the baby is born, the placenta is usually expelled from the uterus in a process called afterbirth.
Chorionic Gonadotropin (hCG) is a hormone that is produced during pregnancy. It is produced by the placenta after implantation of the fertilized egg in the uterus. The main function of hCG is to prevent the disintegration of the corpus luteum, which is a temporary endocrine structure that forms in the ovary after ovulation and produces progesterone during early pregnancy. Progesterone is essential for maintaining the lining of the uterus and supporting the pregnancy.
hCG can be detected in the blood or urine as early as 10 days after conception, and its levels continue to rise throughout the first trimester of pregnancy. In addition to its role in maintaining pregnancy, hCG is also used as a clinical marker for pregnancy and to monitor certain medical conditions such as gestational trophoblastic diseases.
Trophoblasts are specialized cells that make up the outer layer of a blastocyst, which is a hollow ball of cells that forms in the earliest stages of embryonic development. In humans, this process occurs about 5-6 days after fertilization. The blastocyst consists of an inner cell mass (which will eventually become the embryo) and an outer layer of trophoblasts.
Trophoblasts play a crucial role in implantation, which is the process by which the blastocyst attaches to and invades the lining of the uterus. Once implanted, the trophoblasts differentiate into two main layers: the cytotrophoblasts (which are closer to the inner cell mass) and the syncytiotrophoblasts (which form a multinucleated layer that is in direct contact with the maternal tissues).
The cytotrophoblasts proliferate and fuse to form the syncytiotrophoblasts, which have several important functions. They secrete enzymes that help to degrade and remodel the extracellular matrix of the uterine lining, allowing the blastocyst to implant more deeply. They also form a barrier between the maternal and fetal tissues, helping to protect the developing embryo from the mother's immune system.
Additionally, trophoblasts are responsible for the formation of the placenta, which provides nutrients and oxygen to the developing fetus and removes waste products. The syncytiotrophoblasts in particular play a key role in this process by secreting hormones such as human chorionic gonadotropin (hCG), which helps to maintain pregnancy, and by forming blood vessels that allow for the exchange of nutrients and waste between the mother and fetus.
Abnormalities in trophoblast development or function can lead to a variety of pregnancy-related complications, including preeclampsia, intrauterine growth restriction, and gestational trophoblastic diseases such as hydatidiform moles and choriocarcinomas.
Pregnancy is a physiological state or condition where a fertilized egg (zygote) successfully implants and grows in the uterus of a woman, leading to the development of an embryo and finally a fetus. This process typically spans approximately 40 weeks, divided into three trimesters, and culminates in childbirth. Throughout this period, numerous hormonal and physical changes occur to support the growing offspring, including uterine enlargement, breast development, and various maternal adaptations to ensure the fetus's optimal growth and well-being.
Hormones are defined as chemical messengers that are produced by endocrine glands or specialized cells and are transported through the bloodstream to tissues and organs, where they elicit specific responses. They play crucial roles in regulating various physiological processes such as growth, development, metabolism, reproduction, and mood. Examples of hormones include insulin, estrogen, testosterone, adrenaline, and thyroxine.
Thyroid hormones are hormones produced and released by the thyroid gland, a small endocrine gland located in the neck that helps regulate metabolism, growth, and development in the human body. The two main thyroid hormones are triiodothyronine (T3) and thyroxine (T4), which contain iodine atoms. These hormones play a crucial role in various bodily functions, including heart rate, body temperature, digestion, and brain development. They help regulate the rate at which your body uses energy, affects how sensitive your body is to other hormones, and plays a vital role in the development and differentiation of all cells of the human body. Thyroid hormone levels are regulated by the hypothalamus and pituitary gland through a feedback mechanism that helps maintain proper balance.
Follicle-Stimulating Hormone (FSH) is a glycoprotein hormone secreted and released by the anterior pituitary gland. In females, it promotes the growth and development of ovarian follicles in the ovary, which ultimately leads to the maturation and release of an egg (ovulation). In males, FSH stimulates the testes to produce sperm. It works in conjunction with luteinizing hormone (LH) to regulate reproductive processes. The secretion of FSH is controlled by the hypothalamic-pituitary-gonadal axis and its release is influenced by the levels of gonadotropin-releasing hormone (GnRH), estrogen, inhibin, and androgens.
Luteinizing Hormone (LH) is a glycoprotein hormone, which is primarily produced and released by the anterior pituitary gland. In women, a surge of LH triggers ovulation, the release of an egg from the ovaries during the menstrual cycle. During pregnancy, LH stimulates the corpus luteum to produce progesterone. In men, LH stimulates the testes to produce testosterone. It plays a crucial role in sexual development, reproduction, and maintaining the reproductive system.
Parathyroid hormone (PTH) is a polypeptide hormone that plays a crucial role in the regulation of calcium and phosphate levels in the body. It is produced and secreted by the parathyroid glands, which are four small endocrine glands located on the back surface of the thyroid gland.
The primary function of PTH is to maintain normal calcium levels in the blood by increasing calcium absorption from the gut, mobilizing calcium from bones, and decreasing calcium excretion by the kidneys. PTH also increases phosphate excretion by the kidneys, which helps to lower serum phosphate levels.
In addition to its role in calcium and phosphate homeostasis, PTH has been shown to have anabolic effects on bone tissue, stimulating bone formation and preventing bone loss. However, chronic elevations in PTH levels can lead to excessive bone resorption and osteoporosis.
Overall, Parathyroid Hormone is a critical hormone that helps maintain mineral homeostasis and supports healthy bone metabolism.
Gonadotropin-Releasing Hormone (GnRH), also known as Luteinizing Hormone-Releasing Hormone (LHRH), is a hormonal peptide consisting of 10 amino acids. It is produced and released by the hypothalamus, an area in the brain that links the nervous system to the endocrine system via the pituitary gland.
GnRH plays a crucial role in regulating reproduction and sexual development through its control of two gonadotropins: follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These gonadotropins, in turn, stimulate the gonads (ovaries or testes) to produce sex steroids and eggs or sperm.
GnRH acts on the anterior pituitary gland by binding to its specific receptors, leading to the release of FSH and LH. The hypothalamic-pituitary-gonadal axis is under negative feedback control, meaning that when sex steroid levels are high, they inhibit the release of GnRH, which subsequently decreases FSH and LH secretion.
GnRH agonists and antagonists have clinical applications in various medical conditions, such as infertility treatments, precocious puberty, endometriosis, uterine fibroids, prostate cancer, and hormone-responsive breast cancer.
Gonadal steroid hormones, also known as gonadal sex steroids, are hormones that are produced and released by the gonads (i.e., ovaries in women and testes in men). These hormones play a critical role in the development and maintenance of secondary sexual characteristics, reproductive function, and overall health.
The three main classes of gonadal steroid hormones are:
1. Androgens: These are male sex hormones that are primarily produced by the testes but also produced in smaller amounts by the ovaries and adrenal glands. The most well-known androgen is testosterone, which plays a key role in the development of male secondary sexual characteristics such as facial hair, deepening of the voice, and increased muscle mass.
2. Estrogens: These are female sex hormones that are primarily produced by the ovaries but also produced in smaller amounts by the adrenal glands. The most well-known estrogen is estradiol, which plays a key role in the development of female secondary sexual characteristics such as breast development and the menstrual cycle.
3. Progestogens: These are hormones that are produced by the ovaries during the second half of the menstrual cycle and play a key role in preparing the uterus for pregnancy. The most well-known progestogen is progesterone, which also plays a role in maintaining pregnancy and regulating the menstrual cycle.
Gonadal steroid hormones can have significant effects on various physiological processes, including bone density, cognitive function, mood, and sexual behavior. Disorders of gonadal steroid hormone production or action can lead to a range of health problems, including infertility, osteoporosis, and sexual dysfunction.