Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction

The proinflammatory cytokine MIF (macrophage migration inhibitory factor) is involved in physiological and pathological processes in pregnancy. MIF maternal serum levels are increased in preeclampsia (PE). We hypothesize that pregnancy tissues are the source of MIF overexpression in PE. MIF protein...

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Main Authors: Simona Cardaropoli, Luana Paulesu, Roberta Romagnoli, Francesca Ietta, Daniela Marzioni, Mario Castellucci, Alessandro Rolfo, Elena Vasario, Ettore Piccoli, Tullia Todros
Format: Article
Language:English
Published: Wiley 2012-01-01
Series:Clinical and Developmental Immunology
Online Access:http://dx.doi.org/10.1155/2012/639342
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author Simona Cardaropoli
Luana Paulesu
Roberta Romagnoli
Francesca Ietta
Daniela Marzioni
Mario Castellucci
Alessandro Rolfo
Elena Vasario
Ettore Piccoli
Tullia Todros
author_facet Simona Cardaropoli
Luana Paulesu
Roberta Romagnoli
Francesca Ietta
Daniela Marzioni
Mario Castellucci
Alessandro Rolfo
Elena Vasario
Ettore Piccoli
Tullia Todros
author_sort Simona Cardaropoli
collection DOAJ
description The proinflammatory cytokine MIF (macrophage migration inhibitory factor) is involved in physiological and pathological processes in pregnancy. MIF maternal serum levels are increased in preeclampsia (PE). We hypothesize that pregnancy tissues are the source of MIF overexpression in PE. MIF protein was studied in maternal sera, placental tissues, fetal membranes, and umbilical cord of 8 control and 20 PE pregnancies: 10 with normal fetal growth (PE-AGA) and 10 with fetal growth restriction (PE-FGR). MIF levels were significantly higher in PE-AGA membranes than in controls and PE-FGR. In PE-FGR, MIF cord concentrations were higher than in PE-AGA while MIF placental levels were lower than in controls. MIF maternal serum levels were higher in PE, compared to controls, and the difference was mainly due to PE-FGR samples. These data support MIF involvement in PE pathogenesis and suggest that different pregnancy tissues contribute to MIF production in PE with and without fetoplacental compromise.
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institution Kabale University
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language English
publishDate 2012-01-01
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series Clinical and Developmental Immunology
spelling doaj-art-a70dbc2de23943b5b32a1c460d835a8b2025-02-03T01:07:03ZengWileyClinical and Developmental Immunology1740-25221740-25302012-01-01201210.1155/2012/639342639342Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth RestrictionSimona Cardaropoli0Luana Paulesu1Roberta Romagnoli2Francesca Ietta3Daniela Marzioni4Mario Castellucci5Alessandro Rolfo6Elena Vasario7Ettore Piccoli8Tullia Todros9Department of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, ItalyDepartment of Physiology, University of Siena, Via Aldo Moro 4 53100 Siena, ItalyDepartment of Physiology, University of Siena, Via Aldo Moro 4 53100 Siena, ItalyDepartment of Physiology, University of Siena, Via Aldo Moro 4 53100 Siena, ItalyDepartment of Molecular Pathology and Innovative Therapies, Marche Polytechnic University, Via Tronto 10/a 60020 Ancona, ItalyDepartment of Molecular Pathology and Innovative Therapies, Marche Polytechnic University, Via Tronto 10/a 60020 Ancona, ItalyDepartment of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, ItalyDepartment of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, ItalyDepartment of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, ItalyDepartment of Obstetrics and Gynecology, University of Turin, Sant’Anna Hospital, Via Ventimiglia 3, 10126 Torino, ItalyThe proinflammatory cytokine MIF (macrophage migration inhibitory factor) is involved in physiological and pathological processes in pregnancy. MIF maternal serum levels are increased in preeclampsia (PE). We hypothesize that pregnancy tissues are the source of MIF overexpression in PE. MIF protein was studied in maternal sera, placental tissues, fetal membranes, and umbilical cord of 8 control and 20 PE pregnancies: 10 with normal fetal growth (PE-AGA) and 10 with fetal growth restriction (PE-FGR). MIF levels were significantly higher in PE-AGA membranes than in controls and PE-FGR. In PE-FGR, MIF cord concentrations were higher than in PE-AGA while MIF placental levels were lower than in controls. MIF maternal serum levels were higher in PE, compared to controls, and the difference was mainly due to PE-FGR samples. These data support MIF involvement in PE pathogenesis and suggest that different pregnancy tissues contribute to MIF production in PE with and without fetoplacental compromise.http://dx.doi.org/10.1155/2012/639342
spellingShingle Simona Cardaropoli
Luana Paulesu
Roberta Romagnoli
Francesca Ietta
Daniela Marzioni
Mario Castellucci
Alessandro Rolfo
Elena Vasario
Ettore Piccoli
Tullia Todros
Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
Clinical and Developmental Immunology
title Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
title_full Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
title_fullStr Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
title_full_unstemmed Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
title_short Macrophage Migration Inhibitory Factor in Fetoplacental Tissues from Preeclamptic Pregnancies with or without Fetal Growth Restriction
title_sort macrophage migration inhibitory factor in fetoplacental tissues from preeclamptic pregnancies with or without fetal growth restriction
url http://dx.doi.org/10.1155/2012/639342
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