Document Detail

Increased phospholipase A2 and thromboxane but not prostacyclin production by placental trophoblast cells from normal and preeclamptic pregnancies cultured under hypoxia condition.
MedLine Citation:
PMID:  15850645     Owner:  NLM     Status:  MEDLINE    
In this study we determined whether hypoxia could promote vasoactivator thromboxane (TX) and prostacyclin (PGI2) as well as phospholipase A2 (PLA2) production by placental trophoblast cells (TCs) from normal and preeclamptic (PE) pregnancies. Placentas were obtained immediately after delivery from normal (n=9) and preeclamptic (n=9) pregnancies. TCs were isolated by dispase digestion of villous tissue and purified by Percoll gradient centrifugation. TCs (5x10(6) cells/well) were cultured with Dulbecco's Modified Eagles Medium (DMEM) under hypoxia condition (2% O2/5% CO2/93% N2) for 48 h. TCs cultured under normoxia condition (5% CO2/air) were used as control. Culture medium was collected at the end of incubation. Productions for TX, PGI2 and PLA2 were measured by ACE competitive enzyme immunoassay (EIA). Comparisons were made using the Mann-Whitney U test or paired t-test and the data are expressed as mean+/-SE (pg/microg cellular protein). Significance was set at a p-value of <0.05. We found: (1) PE-TCs produced more TXB2 and PLA2 than normal-TCs under normoxia conditions, TXB2: 4.33+/-1.03 vs. 1.84+/-0.29 pg/microg protein, p<0.05; PLA2: 0.38+/-0.08 vs. 0.21+/-0.03 pg/microg protein, p<0.05, respectively. (2) Hypoxia promoted both PE- and normal-TCs to generate more TXB2 and PLA2, TXB2: 6.36+/-1.72 vs. 3.05+/-0.45 pg/microg; PLA2: 0.52+/-0.10 vs. 0.30+/-0.04 pg/microg, respectively. (3) No change in 6-keto PGF1alpha production was observed for normal-TCs or PE-TCs when compared under normoxia vs. hypoxia condition, normal-TCs: 0.20+/-0.05 vs. 0.21+/-0.05 pg/microg; PE-TCs: 0.38+/-0.05 vs. 0.36+/-0.04 pg/microg, respectively. We concluded that hypoxia promotes both PLA2 and TX, but not PGI2, production by placental trophoblast cells cultured under hypoxia condition. These results suggest that increased PLA2 release may alter the arachidonic acid cascade and promote TX synthesis. Relative hypoxia could contribute to the increase in TX production and result in vasoconstriction in placental vasculature in preeclampsia.
Robin S Bowen; Yanping Zhang; Yang Gu; David F Lewis; Yuping Wang
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Placenta     Volume:  26     ISSN:  0143-4004     ISO Abbreviation:  Placenta     Publication Date:  2005 May 
Date Detail:
Created Date:  2005-04-26     Completed Date:  2005-08-22     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  402-9     Citation Subset:  IM    
Department of Obstetrics and Gynecology, Louisiana State University Health Sciences Center, PO Box 33932, Shreveport, LA 71130, USA.
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MeSH Terms
6-Ketoprostaglandin F1 alpha / biosynthesis
Cell Hypoxia
Cells, Cultured
Epoprostenol / biosynthesis*
Phospholipases A / biosynthesis*
Phospholipases A2
Pre-Eclampsia / metabolism*,  pathology
Thromboxane B2 / biosynthesis
Thromboxanes / biosynthesis*
Trophoblasts / metabolism*
Grant Support
Reg. No./Substance:
0/Thromboxanes; 35121-78-9/Epoprostenol; 54397-85-2/Thromboxane B2; 58962-34-8/6-Ketoprostaglandin F1 alpha; EC 3.1.1.-/Phospholipases A; EC A2

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