Study on reproductive endocrinology of human placenta (II)--Hormone secreting activity of cytotrophoblast cells.
ABSTRACT The capability of cytotrophoblast cells to produce hCG, progesterone, estrogen, cGnRH and beta-endorphin in vitro has been demonstrated in serum-free culture medium. Before experiment, a 24-h preculture was carried out in order to remove the endogenous hormones of the tissue. During a period of 8 days' culture, the cytotrophoblast cells could constantly produce a small amount of hCG. The production of progesterone rose rapidly and became doubled within six days. The estrogen secretion showed a similar pattern in the presence of androstenedione, a precursor of estrogen, indicating the elevation of aromatase activity in the cells. The elevation of the enzyme activity has been further demonstrated not to be induced by androstenedione. In both cytotrophoblast and syncytiotrophoblast cell cultures, cGnRH was only detected in the culture of cytotrophoblast cells, with a value up to 4 pg/10(5) cells/24 h. However, beta-endorphin was identified both in cytotrophoblast and syncytiotrophoblast cells. Its content increased significantly in the medium of cytotrophoblast cell culture from the 4th to 6th days, but declined in the medium of syncytiotrophoblast cell culture. The results demonstrate clearly that the cytotrophoblast cells are the sole origin of GnRH in human placenta and are also able to synthesize beta-endorphin and steroid hormones. The findings indicate that there is no such a sharp functional demarcation existing between these two kinds of trophoblast cells as suggested before. The data are of significance for a better understanding of the mechanism of hormonal regulation in placenta.
SourceAvailable from: Craig S AtwoodEmbryonic Stem Cells: The Hormonal Regulation of Pluripotency and Embryogenesis, 04/2011; , ISBN: 978-953-307-196-1
Hormones in Neurodegeneration, Neuroprotection, and Neurogenesis, 02/2011: pages 305 - 329; , ISBN: 9783527633968
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ABSTRACT: In response to stress corticotropin releasing hormone (CRH) is secreted from the hypothalamus and travels to the anterior pituitary where it stimulates the release of proteins derived from the precursor protein, proopiomelanocortin (POMC), including adrenocorticotropic hormone (ACTH) and -endorphin. -endorphin interacts with opioid receptors and relieves stress while ACTH travels through the blood stream to the adrenal cortex where it stimulates the release of cortisol. Cortisol's actions include releasing glucose from stored glycogen and stimulating breakdown of fat from adipose tissue, induction of gluconeogenesis and modulation of the immune system. As a negative feedback control, cortisol inhibits CRH release from the hypothalamus and ACTH from the anterior pituitary. During pregnancy the placenta synthesizes and secretes CRH into the systemic circulation causing a dramatic increase in the circulating levels of CRH throughout pregnancy that peaks at delivery and unlike the situation in the hypothalamus, cortisol has a positive effect on placental CRH production. While the CRH binding protein (CRH-BP) may attenuate the action of placental CRH on the pregnant woman's pituitary, there is evidence that the CRH-BP does not completely cut off access of placental CRH to the pituitary. For example, CRH-BP levels decrease in late pregnancy lowering the ability to decrease CRH activity. In late pregnancy when circulating CRH levels rise dramatically and superimpose over falling levels of the CRH-BP, the anterior pituitary may desensitize to placental CRH so that ACTH and cortisol levels do not become pathologically elevated. In non-pregnant individuals, disturbances in the hypothalamic CRH -pituitary ACTH axis are associated with mood disturbances and in pregnant women who have elevated CRH levels during pregnancy an association with prenatal depression has been shown. More work needs to be done to investigate the possible roles of CRH in pregnancy related depression. Besides effects on the pituitary, placental CRH may exert physiological regulation on the uterus. Higher than normal levels of CRH in mid-pregnancy are associated with preterm pregnancy suggesting a role for CRH in the timing of parturition. In preterm pregnancy when the uterus has to be kept quiescent, CRH receptors are coupled to various cell signaling systems including the cyclic AMP system that inhibits myosin light chain phosphorylation in smooth muscle thereby dampening uterine contraction. As the time for labour approaches, CRH receptors may alter coupling to cellular signaling systems that phosphorylate myosin light chain and initiate rhythmic contraction of the uterus. The possibility of using modulators of CRH action such as CRH receptor agonists to correct pathological conditions in the expectant mother provides a powerful motivation for future studies to fully elucidate the roles of CRH in pregnancy.Current Women s Health Reviews 11/2008; 4(4):270-279. DOI:10.2174/157340408786848197