Biologically active corticotropin-releasing hormone in maternal and fetal plasma during pregnancy

Goland, Robin; Wardlaw, Sharon L.; Blum, Mariann; Tropper, Pamela; Stark, Raymond I.

doi:10.1016/s0002-9378(88)80162-5

Cited by 164 publications

(76 citation statements)

References 14 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The high expression of the CRH gene observed in placenta is in agreement with earlier findings, which describe this organ as the main source of intrauterine CRH protein production (Shibasaki et al 1982, Goland et al 1988, Sasaki et al 1988, Glynn et al 1998). To date, the possible quantitative contribution of other gestational tissues to intrauterine CRH synthesis has hardly been addressed.…”

Section: Discussionsupporting

confidence: 92%

mRNA expression profiles for corticotrophin-releasing hormone, urocortin, CRH-binding protein and CRH receptors in human term gestational tissues determined by real-time quantitative RT-PCR

Sehringer

Hp²,

Simon³

et al. 2004

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

Increasing maternal plasma levels of corticotrophin-releasing hormone (CRH) during the last weeks of pregnancy suggest that this stress hormone plays an important role in the control of human parturition. Little is known about the quantitative contribution of gestational tissues (other than placenta) to intrauterine formation of CRH, urocortin and CRH-binding protein (CRH-BP), or about the distribution of CRH receptors within the uterus.We have investigated the mRNA expression of CRH, urocortin, CRH-BP and CRH receptors 1 and 2 (CRH-R1 and -R2) in gestational tissues by real-time RT-PCR. Placenta, myometrium and choriodecidua were collected after uncomplicated pregnancies at term, before the onset of labour. Distribution of CRH-R1 and CRH-R2 protein was also investigated by immunostaining with receptor subtype-specific antibodies.The placenta was identified as the main site of CRH and CRH-BP mRNA expression, displaying mRNA levels >1000 and >20 times higher than those found in the myometrium and choriodecidua respectively (P<0·05 in each case). mRNA expression of urocortin was low in all tissues investigated. Myometrium and choriodecidua expressed relevant amounts of both receptor subtypes, whereas the CRH receptor population in placenta consisted mainly of CRH-R2.The high expression of CRH in placenta and the substantial expression of CRH receptors in choriodecidua and myometrium suggested that CRH derived from placenta exerts direct or indirect actions on these tissues. Neither CRH produced by myometrium or choriodecidua nor urocortin from other intrauterine sources seem to play a major role in the control of labour.

show abstract

Section: Discussionsupporting

confidence: 92%

mRNA expression profiles for corticotrophin-releasing hormone, urocortin, CRH-binding protein and CRH receptors in human term gestational tissues determined by real-time quantitative RT-PCR

Sehringer

Hp²,

Simon³

et al. 2004

Journal of Molecular Endocrinology

View full text Add to dashboard Cite

show abstract

“…The role of placental-derived CRF in this reprogramming has been thoroughly investigated (reviewed in Avishai-Eliner et al, 2002;Sandman, 2015). Although placental synthesis of CRF in rodents has not yet been demonstrated, the human placenta produces CRF beginning in the seventh gestational week, the levels of which exponentially increase in the maternal circulation as pregnancy progresses (Emanuel et al, 1994;Goland et al, 1988;Petraglia et al, 1987;Robinson et al, 1989). Placental CRF is also released into the fetal circulation, where it has influence on nervous system development including regulation of proliferation and survival of neural progenitors (Koutmani et al, 2013).…”

Section: Endocrine Actionmentioning

confidence: 99%

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Bronson

Bale

2015

Neuropsychopharmacol

211

180

View full text Add to dashboard Cite

Adversity experienced during gestation is a predictor of lifetime neuropsychiatric disease susceptibility. Specifically, maternal stress during pregnancy predisposes offspring to sex-biased neurodevelopmental disorders, including schizophrenia, attention deficit/hyperactivity disorder, and autism spectrum disorders. Animal models have demonstrated disease-relevant endophenotypes in prenatally stressed offspring and have provided unique insight into potential programmatic mechanisms. The placenta has a critical role in the deleterious and sex-specific effects of maternal stress and other fetal exposures on the developing brain. Stress-induced perturbations of the maternal milieu are conveyed to the embryo via the placenta, the maternal-fetal intermediary responsible for maintaining intrauterine homeostasis. Disruption of vital placental functions can have a significant impact on fetal development, including the brain, outcomes that are largely sex-specific. Here we review the novel involvement of the placenta in the transmission of the maternal adverse environment and effects on the developing brain.

show abstract

“…48 CRH is produced in increasing concentrations by the placenta throughout gestation, resulting in maternal and fetal serum CRH concentrations at term that are far higher than at any other time in life. 49 Like CRH from the hypothalamus, placental CRH stimulates cortisol production in the fetal adrenal gland. However, in contrast to hypothalamic CRH, which is inhibited by cortisol, placental CRH production is further stimulated by cortisol, resulting in a 'feed-forward' loop of increasing production of cortisol and CRH.…”

Section: Clinical Evidencementioning

confidence: 99%

Relative adrenal insufficiency in the preterm and term infant

2009

View full text Add to dashboard Cite

Cortisol release in the face of illness or stress is vital for survival. Relative adrenal insufficiency occurs when a patient's cortisol response is inadequate for the degree of illness or stress. Numerous studies have documented the existence of relative adrenal insufficiency in critically ill adults, and its association with increased morbidity and mortality. There is increasing evidence that relative adrenal insufficiency may be an etiology for hemodynamic instability and hypotension in the critically ill newborn, but compared with the adult population, there is still a paucity of data in this population. Randomized controlled trials are needed to evaluate the efficacy and safety of glucocorticoids for the treatment of cardiovascular insufficiency due to relative adrenal insufficiency in ill preterm and term newborn infants. Keywords: adrenocorticotropin; ACTH; adrenal insufficiency; corticotrophin-releasing hormone; cortisol; critically ill infants hypothalamic-pituitary-adrenal axis; newborns-full term Introduction Activation of the hypothalamic-pituitary-adrenal (HPA) axis and ultimate release of cortisol are critical in maintaining homeostasis in response to stress. Relative adrenal insufficiency occurs when the HPA axis produces insufficient cortisol for the degree of illness or stress. In some critically ill adult populations, relative adrenal insufficiency is prevalent, 1-4 and is associated with increased morbidity and mortality. 2,3,5 Some studies of glucocorticoid treatment in critically ill adults have shown benefit, with faster reversal of shock and reduction in mortality. 3,[5][6][7][8] Recently, increasing evidence supports the existence of relative adrenal insufficiency in ill newborns, but, similar to other ill populations, there remains no general consensus on which patients should be tested, which tests to use and how to interpret them, which patients should be treated or how they should be treated. 9 The following discussion is an overview of corticosteroid physiology, relative adrenal insufficiency in critically ill populations and evidence of its existence in newborn infants, with proposed underlying

show abstract

Biologically active corticotropin-releasing hormone in maternal and fetal plasma during pregnancy

Cited by 164 publications

References 14 publications

mRNA expression profiles for corticotrophin-releasing hormone, urocortin, CRH-binding protein and CRH receptors in human term gestational tissues determined by real-time quantitative RT-PCR

mRNA expression profiles for corticotrophin-releasing hormone, urocortin, CRH-binding protein and CRH receptors in human term gestational tissues determined by real-time quantitative RT-PCR

The Placenta as a Mediator of Stress Effects on Neurodevelopmental Reprogramming

Relative adrenal insufficiency in the preterm and term infant

Contact Info

Product

Resources

About