Changes in Placental CRH, Urocortins, and CRH-Receptor mRNA Expression Associated with Preterm Delivery and Chorioamnionitis

Torricelli, Michela; Novembri, Romina; Bloise, Enrrico; Bonis, Maria De; Challis, John

doi:10.1210/jc.2010-1740

Cited by 48 publications

(28 citation statements)

References 37 publications

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“…Exclusion criteria included samples from pregnant women experiencing PTD associated with asthma, cardiovascular diseases, cervical incompetence, diabetes, fetal growth restriction, fetal malformation, hypertension, multiple gestation, preeclampsia, sexually transmitted diseases, thyroid disease and uterine malformations [34]. The clinical profiles of all pregnancies enrolled in the study are presented in Table 1.…”

Section: Methodsmentioning

confidence: 99%

Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta

Império

Bloise

Javam³

et al. 2018

Cell Physiol Biochem

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Background/Aims: The ATP-binding cassette (ABC) transporters mediate drug biodisposition and immunological responses in the placental barrier. In vitro infective challenges alter expression of specific placental ABC transporters. We hypothesized that chorioamnionitis induces a distinct pattern of ABC transporter expression. Methods: Gene expression of 50 ABC transporters was assessed using TaqMan® Human ABC Transporter Array, in preterm human placentas without (PTD; n=6) or with histological chorioamnionitis (PTDC; n=6). Validation was performed using qPCR, immunohistochemistry and Western blot. MicroRNAs known to regulate P-glycoprotein (P-gp) were examined by qPCR. Results: Up-regulation of ABCB9, ABCC2 and ABCF2 mRNA was detected in chorioamnionitis (p<0.05), whereas placental ABCB1 (P-gp; p=0.051) and ABCG2 (breast cancer resistance protein-BCRP) mRNA levels (p=0.055) approached near significant up-regulation. In most cases, the magnitude of the effect significantly correlated to the severity of inflammation. Upon validation, increased placental ABCB1 and ABCG2 mRNA levels (p<0.05) were observed. At the level of immunohistochemistry, while BCRP was increased (p<0.05), P-gp staining intensity was significantly decreased (p<0.05) in PTDC. miR-331-5p, involved in P-gp suppression, was upregulated in PTDC (p<0.01) and correlated to the grade of chorioamnionitis (p<0.01). Conclusions: Alterations in the expression of ABC transporters will likely lead to modified transport of clinically relevant compounds at the inflamed placenta. A better understanding of the potential role of these transporters in the events surrounding PTD may also enable new strategies to be developed for prevention and treatment of PTD.

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Section: Methodsmentioning

confidence: 99%

Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta

Império

Bloise

Javam³

et al. 2018

Cell Physiol Biochem

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“…42,43 Recently, studies have shown a significant impact of chorioamnionitis on placental CRH and urocortins and their receptors, suggesting that placental expression of stress-related pathways is activated in infective processes. 44 Even cervical incompetence manifesting as a case of preterm labor, mechanical causes excluded, may be related to infection and inflammation, as a shortened or damaged cervix would not be capable of impeding the ascent of bacteria.…”

Section: Infection and Inflammationmentioning

confidence: 99%

Endocrine, paracrine, and autocrine placental mediators in labor

Iliodromiti¹,

Antonakopoulos²,

Sifakis³

et al. 2012

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considering that preterm birth accounts for about 6-10% of all births in Western countries and of more than 65% of all perinatal deaths, elucidation of the particularly complicated mechanisms of labor is essential for determination of appropriate and effective therapeutic interventions. Labor in humans results from a complex interplay of fetal and maternal factors, which act upon the uterus to trigger pathways leading gradually to a coordinated cervical ripening and myometrial contractility. Although the exact mechanism of labor still remains uncertain, several components have been identified and described in detail. Based on the major role played by the human placenta in pregnancy and the cascade of labor processes activated via placental mediators exerting endocrine, paracrine, and autocrine actions, this review article has aimed at presenting the role of these mediators in term and preterm labor and the molecular pathways of their actions. some of the aforementioned mediators are involved in myometrial activation and preparation and others in myometrial stimulation leading to delivery. In the early stages of pregnancy, myometrial molecules, like progesterone, nitric oxide, and relaxin, contribute to the retention of pregnancy. At late stages of gestation, fetal hypothalamus maturation signals act on the placenta causing the production of hormones, including crH, in an endocrine manner; the signals then enhance paracrinically the production of more hormones, such as estrogens and neuropeptides, that contribute to cervical ripening and uterine contractility. These molecules act directly on the myometrium through specific receptors, while cytokines and multiple growth factors are also produced, additionally contributing to labor. In situations HORMONES 2012, 11(4):397-409 Review

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“…In contrast, urocortin 2 decreased output of proinflammatory cytokines produced in response to the LPS stimulus (Torricelli et al 2011). We found that placental tissue collected from women in preterm labor with chorioamnionitis expressed increased amounts of CRH, urocortin 2 and CRH-receptor 1 compared to tissue from women delivered preterm without infection (Torricelli et al 2011). The same pattern of response was produced with LPS stimulation of the tissue.…”

Section: Placental Neuropeptidesmentioning

confidence: 57%

“…Urocortin synergizes with lipopolysaccharide (LPS) to stimulate output of the proinflammatory cytokine, tumor necrosis factor α, TNFα, by placental cells in vitro. In contrast, urocortin 2 decreased output of proinflammatory cytokines produced in response to the LPS stimulus (Torricelli et al 2011). We found that placental tissue collected from women in preterm labor with chorioamnionitis expressed increased amounts of CRH, urocortin 2 and CRH-receptor 1 compared to tissue from women delivered preterm without infection (Torricelli et al 2011).…”

Section: Placental Neuropeptidesmentioning

confidence: 69%

The Role of the Placenta in Fetal Programming

Challis

Sloboda

et al. 2014

Research and Perspectives in Endocrine Interactions

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The placenta occupies a critical place in fetal programming by modulating fetal responses to alterations in the maternal environment, by regulating transfer of nutrients between mother and fetus and by responding to changes in environmental stimuli that affect maternal and/or fetal physiology. Placental size and function are exquisitely sensitive to alterations in maternal nutrition, oxygen tension and exposure to glucocorticoids. These factors affect the activity of proteins such as

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Changes in Placental CRH, Urocortins, and CRH-Receptor mRNA Expression Associated with Preterm Delivery and Chorioamnionitis

Abstract: Our findings showed a significant impact of pPROM with chorioamnionitis on placental CRH peptides and receptors, suggesting that placental expression of stress-related pathways is activated in infective process.

Cited by 48 publications

References 37 publications

Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta

Chorioamnionitis Induces a Specific Signature of Placental ABC Transporters Associated with an Increase of miR-331-5p in the Human Preterm Placenta

Endocrine, paracrine, and autocrine placental mediators in labor

The Role of the Placenta in Fetal Programming

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