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Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia

BACKGROUND: Preeclampsia (PE) is associated with alterations of placental function. The incidence of PE is higher in insulin resistant states. Women with PE have high circulating levels of the metabolic regulator fibroblast growth factor 21 (FGF21). FGF21 is synthesized in the placenta. The aim of t...

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Autores principales: Dekker Nitert, Marloes, Scholz-Romero, Katherin, Kubala, Marta H, McIntyre, H David, Callaway, Leonie K, Barrett, Helen L
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4384232/
https://www.ncbi.nlm.nih.gov/pubmed/25890271
http://dx.doi.org/10.1186/s12958-015-0006-3
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author Dekker Nitert, Marloes
Scholz-Romero, Katherin
Kubala, Marta H
McIntyre, H David
Callaway, Leonie K
Barrett, Helen L
author_facet Dekker Nitert, Marloes
Scholz-Romero, Katherin
Kubala, Marta H
McIntyre, H David
Callaway, Leonie K
Barrett, Helen L
author_sort Dekker Nitert, Marloes
collection PubMed
description BACKGROUND: Preeclampsia (PE) is associated with alterations of placental function. The incidence of PE is higher in insulin resistant states. Women with PE have high circulating levels of the metabolic regulator fibroblast growth factor 21 (FGF21). FGF21 is synthesized in the placenta. The aim of this study was to compare the expression of FGF21, its receptors, downstream targets and transcriptional regulators in placental tissue from pregnancies with and without late-onset PE. Circulating FGF21 in maternal and cord blood was also studied. METHODS: mRNA expression was determined by semi-quantitative real-time PCR and normalized for cellular composition in 17 women with and 20 without PE. Protein expression was quantified by Western Blot. FGF21 levels were measured by ELISA in maternal and cord serum of ten mother-baby dyads per condition. RESULTS: Placental FGF21 mRNA and protein expression were similar in PE compared with control. Placental mRNA expression of the FGF receptors (1–4) and the co-receptor beta-Klotho was not different between the groups. There was no difference in the expression of the glucose transporters GLUT1, 3 or 4. PPAR-alpha but not PPAR-gamma expression was decreased in PE. Maternal FGF21 serum levels were not significantly different in PE. FGF21 was detected in cord blood of 6 infants (4 PE, 2 controls) but was undetectable in 14 infants. CONCLUSIONS: Late-onset PE is not associated with major changes to the expression of FGF21, its receptors or metabolic targets. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12958-015-0006-3) contains supplementary material, which is available to authorized users.
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spelling pubmed-43842322015-04-04 Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia Dekker Nitert, Marloes Scholz-Romero, Katherin Kubala, Marta H McIntyre, H David Callaway, Leonie K Barrett, Helen L Reprod Biol Endocrinol Research BACKGROUND: Preeclampsia (PE) is associated with alterations of placental function. The incidence of PE is higher in insulin resistant states. Women with PE have high circulating levels of the metabolic regulator fibroblast growth factor 21 (FGF21). FGF21 is synthesized in the placenta. The aim of this study was to compare the expression of FGF21, its receptors, downstream targets and transcriptional regulators in placental tissue from pregnancies with and without late-onset PE. Circulating FGF21 in maternal and cord blood was also studied. METHODS: mRNA expression was determined by semi-quantitative real-time PCR and normalized for cellular composition in 17 women with and 20 without PE. Protein expression was quantified by Western Blot. FGF21 levels were measured by ELISA in maternal and cord serum of ten mother-baby dyads per condition. RESULTS: Placental FGF21 mRNA and protein expression were similar in PE compared with control. Placental mRNA expression of the FGF receptors (1–4) and the co-receptor beta-Klotho was not different between the groups. There was no difference in the expression of the glucose transporters GLUT1, 3 or 4. PPAR-alpha but not PPAR-gamma expression was decreased in PE. Maternal FGF21 serum levels were not significantly different in PE. FGF21 was detected in cord blood of 6 infants (4 PE, 2 controls) but was undetectable in 14 infants. CONCLUSIONS: Late-onset PE is not associated with major changes to the expression of FGF21, its receptors or metabolic targets. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/s12958-015-0006-3) contains supplementary material, which is available to authorized users. BioMed Central 2015-03-08 /pmc/articles/PMC4384232/ /pubmed/25890271 http://dx.doi.org/10.1186/s12958-015-0006-3 Text en © Dekker Nitert et al.; licensee BioMed Central. 2015 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research
Dekker Nitert, Marloes
Scholz-Romero, Katherin
Kubala, Marta H
McIntyre, H David
Callaway, Leonie K
Barrett, Helen L
Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title_full Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title_fullStr Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title_full_unstemmed Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title_short Placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
title_sort placental fibroblast growth factor 21 is not altered in late-onset preeclampsia
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4384232/
https://www.ncbi.nlm.nih.gov/pubmed/25890271
http://dx.doi.org/10.1186/s12958-015-0006-3
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