ArticleMolecular biology reports2015
Assessment of placental and maternal stress responses in patients with pregnancy related complications via monitoring of heat shock protein mRNA levels.
Article in Molecular biology reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 21 citations in OpenAlex.
- Physiological mechanisms of the impact of heat during pregnancy and the clinical implications: review of the evidence from an expert group meeting.International journal of biometeorology · 2022Review
- Pandemic stress and SARS-CoV-2 infection are associated with pathological changes at the maternal-fetal interface.Placenta · 2021Article
- Differential Methylation in Promoter Regions of the GenesFrontiers in medicine · 2020Article
- Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.Neuroscience letters · 2019Review
- Quantification of Calcyclin and Heat Shock Protein 90 in Sera from Women with and without Preeclampsia by Mass Spectrometry.Proteomics. Clinical applications · 2019Article
- Effects ofJournal of Taibah University Medical Sciences · 2018Article
- Consensus strategy in genes prioritization and combined bioinformatics analysis for preeclampsia pathogenesis.BMC medical genomics · 2017Article
- Interaction between the inducible 70-kDa heat shock protein and autophagy: effects on fertility and pregnancy.Cell stress & chaperones · 2015Review
- Expression profile of C19MC microRNAs in placental tissue in pregnancy-related complications.DNA and cell biology · 2015Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The study describes the stress response in the central cotyledon zone of placental tissue and in maternal whole peripheral blood to pregnancy related complications including gestational hypertension (n = 31), preeclampsia w or w/o fetal growth restriction (n = 95), and fetal growth restriction (n = 39) using real-time RT-PCR and genes encoding Hsp27, Hsp60, Hsp70, Hsp90 and HspBP1 proteins. The placental tissue does not respond to pregnancy induced hypertension, fetal growth restriction and short-term severe preeclampsia that requires immediate termination of gestation. Upregulation of Hsp27, Hsp90 and HspBP1 appears just in case of long-term deteriorated conditions (usually in mild preeclampsia, that enable further continuation of gestation, when properly treated). On the other hand, maternal circulation is able to reflect both maternal and fetal pathologic conditions. While pregnancy related complications always induce upregulation of Hsp70 and downregulation of Hsp90 in maternal whole peripheral blood, the increase of Hsp60 mRNA levels occurs entirely in patients with preeclampsia and/or fetal growth restriction. Hsp60, Hsp70 and Hsp90 are dysregulated in maternal circulation irrespective of the severity of the disease (in both mild and severe preeclampsia) and the requirements for the delivery (before and after 34th week of gestation). Nevertheless, the highest Hsp60 mRNA levels may be observed in pregnancies with signs of the centralization of the fetal circulation associated with fetal hypoxia.
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