PubTransformer

A site to transform Pubmed publications into these bibliographic reference formats: ADS, BibTeX, EndNote, ISI used by the Web of Knowledge, RIS, MEDLINE, Microsoft's Word 2007 XML.

Inflammation-induced fetal growth restriction in rats is associated with increased placental HIF-1α accumulation.

Abstract Hypoxia-inducible factor 1-alpha (HIF-1α) is the oxygen-sensitive subunit of the transcription factor HIF-1, and its expression is increased in placentas from pregnancies complicated by pre-eclampsia (PE). Fetal growth restriction (FGR) and PE often share a common pathophysiology; however, it is unknown whether increased placental HIF-1α occurs in FGR. We previously demonstrated that aberrant maternal inflammation in rats resulted in altered utero-placental perfusion and FGR, both of which were prevented by administration of the nitric oxide mimetic glyceryl trinitrate (GTN). Our aim here was to determine whether abnormal maternal inflammation causing FGR is linked to placental HIF-1α accumulation and whether GTN administration could prevent increases in placental HIF-1α.
PMID
Related Publications

Hypoxia-independent upregulation of placental hypoxia inducible factor-1α gene expression contributes to the pathogenesis of preeclampsia.

Comparison of maternal and umbilical cord blood HIF-1α and nitric oxide levels in early and late onset preeclamptic pregnancies.

Inflammation-induced fetal growth restriction in rats is associated with altered placental morphometrics.

Inflammation in rat pregnancy inhibits spiral artery remodeling leading to fetal growth restriction and features of preeclampsia.

Proteasomal activity in placentas from women with preeclampsia and intrauterine growth restriction: implications for expression of HIF-alpha proteins.

Authors

Mayor MeshTerms
Keywords
Journal Title plos one
Publication Year Start




PMID- 28423052
OWN - NLM
STAT- In-Process
DA  - 20170419
LR  - 20170419
IS  - 1932-6203 (Electronic)
IS  - 1932-6203 (Linking)
VI  - 12
IP  - 4
DP  - 2017
TI  - Inflammation-induced fetal growth restriction in rats is associated with
      increased placental HIF-1alpha accumulation.
PG  - e0175805
LID - 10.1371/journal.pone.0175805 [doi]
AB  - INTRODUCTION: Hypoxia-inducible factor 1-alpha (HIF-1alpha) is the
      oxygen-sensitive subunit of the transcription factor HIF-1, and its expression is
      increased in placentas from pregnancies complicated by pre-eclampsia (PE). Fetal 
      growth restriction (FGR) and PE often share a common pathophysiology; however, it
      is unknown whether increased placental HIF-1alpha occurs in FGR. We previously
      demonstrated that aberrant maternal inflammation in rats resulted in altered
      utero-placental perfusion and FGR, both of which were prevented by administration
      of the nitric oxide mimetic glyceryl trinitrate (GTN). Our aim here was to
      determine whether abnormal maternal inflammation causing FGR is linked to
      placental HIF-1alpha accumulation and whether GTN administration could prevent
      increases in placental HIF-1alpha. METHODS: Levels of inflammatory factors in
      maternal plasma were measured using a multiplex assay after an injection of
      low-dose lipopolysaccharide (LPS) to rats on gestational day (GD) 13.5. Following
      three additional daily LPS injections from GD14.5-16.5, GD17.5 placentas were
      harvested for HIF-1alpha immunolocalisation; serial sections were also stained
      for the hypoxia marker pimonidazole. A subset of rats received LPS injections
      along with GTN delivered continuously (25 mug/h via a transdermal patch) on
      GD12.5-GD17.5. RESULTS: Within two hours of LPS administration, levels of
      maternal pro-inflammatory cytokines were increased compared with saline-treated
      controls. GD17.5 placentas of growth-restricted fetuses exhibited increased
      HIF-1alpha accumulation; however, this did not correlate with pimonidazole
      staining for which no differences were observed between groups. Furthermore, the 
      LPS-mediated increases in maternal inflammatory cytokine levels and placental
      HIF-1alpha accumulation did not occur in rats treated with GTN. DISCUSSION: Our
      results demonstrate that inflammation-induced FGR is associated with increased
      placental HIF-1alpha accumulation; however, expression of this transcription
      factor may not correlate with regions of hypoxia in late-gestation placentas. The
      GTN-mediated attenuation of placental HIF-1alpha accumulation in LPS-treated rats
      provides insight into the mechanism by which GTN improves inflammation-induced
      complications of pregnancy.
FAU - Robb, Kevin P
AU  - Robb KP
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston,
      Ontario, Canada.
FAU - Cotechini, Tiziana
AU  - Cotechini T
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston,
      Ontario, Canada.
FAU - Allaire, Camille
AU  - Allaire C
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston,
      Ontario, Canada.
FAU - Sperou, Arissa
AU  - Sperou A
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston,
      Ontario, Canada.
FAU - Graham, Charles H
AU  - Graham CH
AD  - Department of Biomedical and Molecular Sciences, Queen's University, Kingston,
      Ontario, Canada.
LA  - eng
PT  - Journal Article
DEP - 20170419
PL  - United States
TA  - PLoS One
JT  - PloS one
JID - 101285081
EDAT- 2017/04/20 06:00
MHDA- 2017/04/20 06:00
CRDT- 2017/04/20 06:00
PHST- 2016/07/03 [received]
PHST- 2017/03/31 [accepted]
AID - 10.1371/journal.pone.0175805 [doi]
AID - PONE-D-16-26639 [pii]
PST - epublish
SO  - PLoS One. 2017 Apr 19;12(4):e0175805. doi: 10.1371/journal.pone.0175805.
      eCollection 2017.

<?xml version="1.0" encoding="UTF-8"?>
<b:Sources SelectedStyle="" xmlns:b="http://schemas.openxmlformats.org/officeDocument/2006/bibliography"  xmlns="http://schemas.openxmlformats.org/officeDocument/2006/bibliography" >
</b:Sources>