Transcriptional Regulation of Human Placental Corticotropin-Releasing Factor by Prostaglandins and Estradiol1

Dibbs, Khaled I.; Anteby, Eyal Y.; Mallon, Mary Ann; Sadovsky, Yoel; Adler, Stuart B.

doi:10.1095/biolreprod57.6.1285

Cited by 29 publications

(10 citation statements)

References 50 publications

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“…In the placenta and fetal membranes, the production of PGE 2 and PGF 2a was enhanced by CRH in vitro (Jones and Challis, 1989). Since PGE 2 (Dibbs et al, 1997) and interleukin 1b (Petraglia et al, 1990) themselves increase the CRH synthesis of trophoblast cells, this may constitute a positive paracrine feedback loop resulting in labour and delivery. In addition, CRH stimulates the synthesis of oxytocin in the placenta (Florio et al, 1996).…”

Section: Discussionmentioning

confidence: 99%

Expression Patterns of CRH, CRH Receptors, and CRH Binding Protein in Human Gestational Tissue at Term

Wetzka¹,

Sehringer²,

Wr³

et al. 2003

Exp Clin Endocrinol Diabetes

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Recent research suggests a significant role for placental corticotropin-releasing hormone (CRH) in controlling human parturition. This paper describes the expression of CRH, CRH receptors 1 and 2, and CRH binding protein (CRH-BP) in gestational tissue in late pregnancy. Placenta, myometrium, decidua, and fetal membranes were collected after uncomplicated pregnancies at term caesarian section before the onset of labour. The localisation and mRNA expression of CRH, CRH receptors, and CRH-BP were studied by immunohistochemistry and reverse transcription (RT)-PCR. CRH receptors were detected in placenta, myometrium, decidua, and fetal membranes. We demonstrated for the first time the presence of CRH receptors on resident macrophages and on endothelial cells. CRH receptor 1 mRNA was detected in all tissues investigated by RT-PCR, whereas CRH receptor 2 mRNA was restricted to myometrium and decidua. CRH mRNA was widely expressed in all tissue under study. Novel findings are also presented on the expression of CRH-BP in the myometrium. This widespread expression of the CRH system in gestational tissue suggests a paracrine role for CRH in the birth process (e.g. effects on macrophages and endothelial cells).

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Section: Discussionmentioning

confidence: 99%

Expression Patterns of CRH, CRH Receptors, and CRH Binding Protein in Human Gestational Tissue at Term

Wetzka¹,

Sehringer²,

Wr³

et al. 2003

Exp Clin Endocrinol Diabetes

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“…Another possible site of action of prostaglandins on the CRH promoter is the cAMP response element (CRE), located at –224, and its binding protein CREB [25]. Indeed, transfection experiments showed that, in choriocarcinoma cell lines transfected with the CRH promoter linked to luciferase, PGE 2 stimulated the activity of the promoter via a cAMP-dependent pathway [41]. The ability of the CRE motif to mediate the effects of prostaglandins on gene expression is further supported by findings on other prostaglandin-regulated genes.…”

Section: Discussionmentioning

confidence: 99%

The Transcription of Corticotropin-Releasing Hormone in Human Endometrial Cells Is Regulated by Cytokines

Makrigiannakis

Margioris²,

Zoumakis³

et al. 1999

Neuroendocrinology

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Corticotropin-releasing hormone (CRH), a hypothalamic neuropeptide, is also produced in the human endometrium where it participates in local inflammatory phenomena associated with the decidualization of endometrial stroma and the implantation of the fertilized egg. The inflammatory cytokines interleukin 1 (IL-1), IL-6 and leukemia inhibitory factor (LIF) appear to be the dominant local regulators of these intrauterine inflammatory processes. In the present study we have examined the direct interactions between cytokines and CRH in the endometrium. For this purpose we have measured the effects of IL-1, IL-6 and LIF on the activity of CRH promoter inserted in human endometrial cells in culture. Homologous transient transfection experiments were conducted employing a 0.9-kb fragment of the 5′ flanking region of the human CRH gene coupled to the luciferase reporter gene, using Ishikawa human endometrial cells. We have found that IL-1β increased the activity of CRH gene promoter, in a time- and dose-dependent manner. This effect was antagonized by the IL-1 receptor antagonist IL-1ra and blocked completely by the cyclo-oxygenase inhibitor indomethacin. Similarly, IL-6 increased the activity of CRH promoter in a dose-dependent fashion, an effect partially reversed by indomethacin. LIF did not have any apparent effect. In conclusion, our data suggest that IL-1 and IL-6 exert a strong stimulatory effect on the expression of endometrial CRH. This effect is most probably mediated via prostaglandins. Based on these data we hypothesize that in the human endometrium interleukins, prostaglandins and CRH form a local network regulating the inflammatory phenomena taking place within the uterine cavity.

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“…moreover, women in the midluteal phase, when both progesterone and estrogen levels are relatively high, show enhanced aCTH levels in response to a stressor [32]. estrogens acting centrally, including in the pituitary corticotrophs and hypothalamus, are able to modulate the stress responses [33], and direct estrogenic regulation of CRF gene expression has been demonstrated in various tissues [34,35]. estrogen would regulate the HPa axis by stimulation of CRF gene expression in the hypothalamus in vivo, since high levels of estrogen replacement increases basal levels of CRF mRNa in the PVN of ovariectomized rats [30].…”

Section: Involvement Of Estrogen On Crf Gene Transcriptionmentioning

confidence: 99%

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

Kageyama

Suda

2009

Endocr J

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Abstract. The hypothalamic-pituitary-adrenal (HPa) axis is activated under various stressors. Corticotropin-releasing factor (CRF) plays a central role in controlling stress response, and regulating the HPa axis. CRF, produced in the hypothalamic paraventricular nucleus (PVN), stimulates adrenocorticotropic hormone (aCTH) production via CRF receptor type 1 (CRF 1 receptor) from the corticotrophs of the anterior pituitary (aP). Cyclic amP (camP)-protein kinase a (PKa) pathway takes a main role in stimulating CRF gene transcription. Forskolin and pituitary adenylate cyclaseactivating polypeptide (PaCaP) stimulate adenylate cyclase, intracellular camP production, and then CRF and arginine vasopressin (aVP) gene expression in hypothalamic 4B cells. Interleukin (IL)-6, produced in the PVN, both directly and indirectly stimulates CRF and aVP gene expression. estradiol may enhance the activation of CRF gene expression in response to stress. The HPa axis is regulated by a negative feedback mechanism, because glucocorticoids inhibit both CRF production in the hypothalamic PVN and aCTH production in the pituitary. Hypothalamic parvocellular neurons in the PVN are known to express glucocorticoid receptors, and glucocorticoids are able to regulate CRF gene transcription and expression levels directly in the PVN. glucocorticoids-dependent repression of camP-stimulated CRF promoter activity is mainly localized to promoter sequences between -278 and -233 bp. Both negative glucocorticoid regulatory element (ngRe) and serum response element (SRe) are involved in the repression of the CRF gene in the hypothalamic cells. Stimulation of crF gene in the hypothalamus Involvement of cAMP on CRF gene transcriptionCyclic amP (camP)-protein kinase a (PKa) pathway takes a main role in stimulating CRF synthesis [3][4][5]. There are several candidates for activating CRF neurons. For example, pituitary adenylate cyclase-activating polypeptide (PaCaP), a member of the secretin/glucagon/vasoactive intestinal peptide (VIP) family, is one of the putative hormones. Both PaCaP and the PaCaP-selective PaCaP receptor type 1 (PaC1 receptor) are known to be highly expressed in the hypothalamus, including the parvocellular and magnocellular subdivisions of the PVN, and the supraoptic nucleus (SON) [6,7]. PaCaP has shown to stimulate camP production in the aP [8]. PaCaP also increases CRF mRNa levels in the parvocellular region of the PVN, suggesting that PaCaP is involved in the positive regulation of CRF gene expression [9].

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Transcriptional Regulation of Human Placental Corticotropin-Releasing Factor by Prostaglandins and Estradiol1

Cited by 29 publications

References 50 publications

Expression Patterns of CRH, CRH Receptors, and CRH Binding Protein in Human Gestational Tissue at Term

Expression Patterns of CRH, CRH Receptors, and CRH Binding Protein in Human Gestational Tissue at Term

The Transcription of Corticotropin-Releasing Hormone in Human Endometrial Cells Is Regulated by Cytokines

Regulatory Mechanisms Underlying Corticotropin-Releasing Factor Gene Expression in the Hypothalam

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