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Cited by 29Pregnancy and preeclampsia studiesReproductive System and PregnancyNeurological Complications and Syndromes

Aberrant expression of corticotropin-releasing hormone in pre-eclampsia induces expression of FasL in maternal macrophages and extravillous trophoblast apoptosis

Petsas, G., Jeschke, U., Richter, D. U., Minas, V., Hammer, A., Kalantaridou, S., Toth, B., Tsatsanis, C. +2 more·2012·Molecular Human Reproduction
DOI 10.1093/molehr/gas027
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Abstract

Corticotropin-releasing hormone (CRH) and its receptors are expressed in human placenta. Recently, the impaired function of this system has been associated with a number of complications of pregnancy, including pre-eclampsia. The aim of the study was to test the hypothesis that CRH participates in the pathophysiology of pre-eclampsia through the induction of macrophage-mediated apoptosis of extravillous trophoblasts (EVTs). We found that the expression of CRH was increased in the EVT of the placental bed biopsy specimens from pre-eclamptic pregnancies (1.8-fold increase; P < 0.05). In addition, significantly larger numbers of apoptotic EVT were detected in pre-eclamptic placentas compared with normal ones (P < 0.05), and only in pre-eclamptic placentas, decidual macrophages were found to be Fas ligand (FasL)-positive. In vitro studies on the effect of CRH on human macrophages suggested that CRH induced the expression of the FasL protein in human macrophages and potentiated their ability to induce the apoptosis of a Fas-expressing EVT-based hybridoma cell line in co-cultures. These findings demonstrate a possible mechanism by which the aberrant expression of CRH in pre-eclampsia may activate the FasL-positive decidual macrophages, impair the physiological turnover of EVT and eventually disturb placentation.

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  • HPA hyperactivity may also contribute to overall preterm birth risk, as some studies link it to placental pathology such as preeclampsia, which raises risk for medically indicated preterm birth.

    “HPA hyperactivity may also underlie overall risk for PTB, as some studies have identified a potential role in placental pathology (e.g., in preeclampsia; Harville et al., 2008; Petsas et al., 2012), which increases risk for medically-indicated PTB.”

    From Childhood stress and birth timing among African American women: cortisol as biological mediator (2017) · cites this paper as Petsas et al., 2012

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Authors
Petsas, G., Jeschke, U., Richter, D. U., Minas, V., Hammer, A., Kalantaridou, S., Toth, B., Tsatsanis, C., Friese, K., & Makrigiannakis, A.
Affiliations
  • University of Crete (GR)
  • Ludwig-Maximilians-Universität München (DE)
  • University of Rostock (DE)
  • Medical University of Graz (AT)
Corresponding author
Makrigiannakis, A.
ORCID
Venue
Molecular Human Reproduction
Publisher
Oxford University Press (OUP)
Published
2012-07-04
Volume
18
Issue
11
Pages
535-545
ISSN
  • 1360-9947 (ISSN-L)
  • 1460-2407
DOI
10.1093/molehr/gas027
OpenAlex
W2144117624
Cited by
29
References
55
Citations by year
2026: 1 · 2025: 1 · 2023: 1 · 2022: 2 · 2021: 4 · 2020: 1 · 2019: 3 · 2018: 3 · 2017: 7 · 2016: 1 · 2014: 4 · 2013: 1
FWCI
1.92
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular Human Reproduction (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Obstetrics and Gynecology › Pregnancy and preeclampsia studies
  • Life Sciences › Immunology and Microbiology › Immunology › Reproductive System and Pregnancy
  • Health Sciences › Medicine › Psychiatry and Mental health › Neurological Complications and Syndromes
Keywords
corticotropin-releasing factor, preeclampsia, Fas ligand, extravillous trophoblast, trophoblast apoptosis, decidual macrophages, placenta, CRH receptors, placentation
MeSH terms
Corticotropin-Releasing Hormone, Decidua, Female, Humans, Immunohistochemistry, Macrophages, Placentation, Pre-Eclampsia, Pregnancy, Trophoblasts, Blotting, Western, Gene Expression, Apoptosis, Coculture Techniques, Cell Line, Tumor, Fas Ligand Protein

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