Human Placenta, Chorion, Amnion and Decidua Express Different Variants of Corticotropin-Releasing Factor Receptor Messenger RNA

Florio, Pasquale; Franchini, Antonella; Reis, Fernando M.; Pezzani, Ilaria; Ottaviani, Enzo; Petraglia, Felice

doi:10.1053/plac.1999.0461

Cited by 70 publications

(44 citation statements)

References 17 publications

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“…Our preliminary TaqMan PCR findings suggest that CRH-R2 expression in the fundus is more pronounced than in the lower uterine segment. On the basis of these observations, we present a more accurate description of quantitative CRH receptor expression in gestational tissues than previous contributions based on conventional PCR methods (Glynn et al 1998, Stevens et al 1998, Florio et al 2000.…”

Section: Discussionmentioning

confidence: 93%

“…Whereas in previous studies non-quantitative or semi-quantitative methods were applied (e.g. Grino et al 1987, Petraglia et al 1993, 1996, Clifton et al 1998, Watanabe et al 1999, Florio et al 2000, Wetzka et al 2003 we investigated differential mRNA expression patterns by using real-time quantitative RT-PCR. CRH and CRH-BP mRNA was mainly expressed by placenta.…”

Section: Discussionmentioning

confidence: 99%

“…The presence of components of the CRH system has been described previously at both the mRNA and the protein level in many gestational tissues (Riley et al 1991, Petraglia et al 1993, 1996, Clifton et al 1998, Stevens et al 1998, Florio et al 2000, Wetzka et al 2003. However, these findings require further differentiation with regard to quantification of relative expression patterns of CRH, urocortin, CRH-BP, CRH-R1 and CRH-R2.…”

Section: Introductionmentioning

confidence: 89%

“…urocortin) and the expression of CRH receptors have been described in numerous peripheral tissues, e.g. placenta (Sasaki et al 1988, Florio et al 2000, endometrium (Gravanis et al 2001), lymphatic organs or immune cells (Baigent 2001) and skin (Slominski et al 2001). In the central nervous system, CRH attenuates inflammatory reactions via glucocorticoid action.…”

Section: Introductionmentioning

confidence: 99%

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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

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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.

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Section: Discussionmentioning

confidence: 93%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 89%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

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

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“…A total of 2 l cDNA was used for PCR amplification. Oligonucleotide primers of previously published sequences for CRH-R1 and CRH-R2 isoforms (Table I) were used (13,32). Positive controls included human brain pituitary cDNA and the human melanoma SKMEL188 cell line cDNA for the CRH-R1 isoforms (13), human brain cerebral cortex cDNA for CRH-R2␣ (8), and human brain hippocampus cDNA for CRH-R2␤ and CRH-R2␥ (16).…”

Section: Rt-pcr Analysismentioning

confidence: 99%

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

Cao

Papadopoulou

Kempuraj

et al. 2005

The Journal of Immunology

299

252

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Mast cells are critical for allergic reactions, but also for innate or acquired immunity and inflammatory conditions that worsen by stress. Corticotropin-releasing hormone (CRH), which activates the hypothalamic-pituitary-adrenal axis under stress, also has proinflammatory peripheral effects possibly through mast cells. We investigated the expression of CRH receptors and the effects of CRH in the human leukemic mast cell (HMC-1) line and human umbilical cord blood-derived mast cells. We detected mRNA for CRH-R1α, 1β, 1c, 1e, 1f isoforms, as well as CRH-R1 protein in both cell types. CRH-R2α (but not R2β or R2γ) mRNA and protein were present only in human cord blood-derived mast cells. CRH increased cAMP and induced secretion of vascular endothelial growth factor (VEGF) without tryptase, histamine, IL-6, IL-8, or TNF-α release. The effects were blocked by the CRH-R1 antagonist antalarmin, but not the CRH-R2 antagonist astressin 2B. CRH-stimulated VEGF production was mediated through activation of adenylate cyclase and increased cAMP, as evidenced by the fact that the effect of CRH was mimicked by the direct adenylate cyclase activator forskolin and the cell-permeable cAMP analog 8-bromo-cAMP, whereas it was abolished by the adenylate cyclase inhibitor SQ22536. This is the first evidence that mast cells express functional CRH receptors and that CRH can induce VEGF secretion selectively. CRH-induced mast cell-derived VEGF could, therefore, be involved in chronic inflammatory conditions associated with increased VEGF, such as arthritis or psoriasis, both of which worsen by stress.

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The Role of Corticotropin-Releasing Hormone Receptors in Placenta and Fetal Membranes during Human Pregnancy

Karteris

Grammatopoulos

Randeva

et al. 2001

Molecular Genetics and Metabolism

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Human Placenta, Chorion, Amnion and Decidua Express Different Variants of Corticotropin-Releasing Factor Receptor Messenger RNA

Cited by 70 publications

References 17 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

Human Mast Cells Express Corticotropin-Releasing Hormone (CRH) Receptors and CRH Leads to Selective Secretion of Vascular Endothelial Growth Factor

The Role of Corticotropin-Releasing Hormone Receptors in Placenta and Fetal Membranes during Human Pregnancy

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