Hypoxia attenuates PGE(2) but increases prostacyclin and thromboxane production in human term villous trophoblast

Blumenstein, M., Keelan, J. A. and Mitchell, M. D. (2001) Hypoxia attenuates PGE(2) but increases prostacyclin and thromboxane production in human term villous trophoblast. Placenta, 22 6: 519-525. doi:10.1053/plac.2001.0689


Author Blumenstein, M.
Keelan, J. A.
Mitchell, M. D.
Title Hypoxia attenuates PGE(2) but increases prostacyclin and thromboxane production in human term villous trophoblast
Journal name Placenta   Check publisher's open access policy
ISSN 0143-4004
1532-3102
Publication date 2001-07-01
Sub-type Article (original research)
DOI 10.1053/plac.2001.0689
Volume 22
Issue 6
Start page 519
End page 525
Total pages 7
Place of publication London, England
Publisher W.B. Saunders
Language eng
Subject 1103 Clinical Sciences
1114 Paediatrics and Reproductive Medicine
Abstract Prostanoids have been proposed to play a major role in the regulation of uteroplacental blood flow. We examined the effect of hypoxia on the production of prostaglandin E2 (PGE2) thromboxane B2 (TXB2), and prostacyclin (measured as 6-keto-PGF1α) by human term trophoblast cells and villous placental explants. Explants (n=8) and purified trophoblast cells (n=5) were incubated for 24-72 h under either normoxic (21 per cent O2) or hypoxic (2 per cent O2) conditions. In trophoblast monolayer cultures, hypoxia attentuated PGE2 production rates to 52 ± 9.4 per cent (mean ± SEM, P<0.05) but recovered to control rates within 48 h. In villous explants, PGE2 production was significantly decreased after 48 and 72 h of hypoxia versus the normoxic control, accompanied by increased production of 6-keto-PGF1α to 173.9 ± 26.7 per cent after 48 h. TXB2 production was increased to 172.3 ± 25.9 per cent and 653.2 ± 135.7 per cent (P<0.05) control after 48 and 72 h of hypoxia, respectively. These results were confirmed in villous explants (n=3) cultured in the presence of exogenous 10 μM arachidonic acid. Hypoxia had no significant effect on TXB2 and 6-keto-PGF1α in trophoblast cells. In summary, our findings suggest that hypoxia could be responsible for abnormal profiles of prostanoid production commonly observed in women with pre-eclampsia. These results indicate a putative link between hypoxia and compromised placental perfusion. © 2001 Harcourt Publishers Ltd.
Keyword Prostaglandin-H Synthase-2
Endothelial Growth-factor
In-vitro
15-Hydroyprostaglandin Dehydrogenase
Preeclamptic Pregnancies
Placental Prostacyclin
Lipid Peroxides
Expression
Oxygen
Cells
Q-Index Code C1
Q-Index Status Provisional Code
Institutional Status Unknown

Document type: Journal Article
Sub-type: Article (original research)
Collection: UQ Centre for Clinical Research Publications
 
Versions
Version Filter Type
Citation counts: TR Web of Science Citation Count  Cited 17 times in Thomson Reuters Web of Science Article | Citations
Scopus Citation Count Cited 18 times in Scopus Article | Citations
Google Scholar Search Google Scholar
Created: Thu, 26 Aug 2010, 22:46:53 EST