PGE2 and TXA2 Production by Isolated Macrophages from Human Placenta

Wetzka, B.; Clark, Dawn E.; Charnock-Jones, D S; Zahradnik, H. P.; Smith, S. K.

doi:10.1007/978-1-4899-1810-9_88

Cited by 6 publications

(3 citation statements)

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“…Several studies also support an anti‐inflammatory/stabilizing function for HBCs . Cultures of HBCs released prostaglandin E 2 , supported trophoblast function, and suppressed T‐cell responses . Thus, reduced numbers of HBCs in patients with severe preterm PE may play an important role in promoting the pro‐inflammatory, anti‐angiogenic processes characteristically observed in placentas delivered from patients with this pregnancy complication .…”

Section: Discussionmentioning

confidence: 90%

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Decreased Levels of Folate Receptor‐β and Reduced Numbers of Fetal Macrophages (Hofbauer Cells) in Placentas from Pregnancies with Severe Pre‐Eclampsia

Tang

Buhimschi

et al. 2013

American J Rep Immunol

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Problem Preeclampsia (PE), a pregnancy complication of unknown etiology, is a major cause of maternal and fetal mortality and morbidity. Previous studies have described placental genes which are up-regulated in expression in PE, but few studies have addressed placental gene suppression in this syndrome. Method of Study Gene profiling and quantitative reverse transcription PCR (qRTPCR) analyses were used to identify genes down-regulated in placentas from women with severe preterm PE compared to gestational age-matched normotensive controls with spontaneous preterm birth (sPTB). Western blotting and immunohistochemistry were used to evaluate levels and patterns of cell type-specific protein expression in PE and sPTB group placentas. Results Levels of macrophage marker [folate receptor (FR)-β, CD163, and CD68] mRNA and FR-β protein were significantly down-regulated in PE group placentas compared to the sPTB group. Numbers of Hofbauer cells (HBCs, fetal macrophages) and FR-β protein in these cells were reduced in PE group placentas. Conclusion Severe PE is associated with decreased placental expression of FR-β and a reduction in the number of HBCs. Reduced placental macrophage function is likely to play a key role in the pathophysiology of PE.

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Section: Discussionmentioning

confidence: 90%

“…Thus, folate deficiency may be expected to exacerbate placental damage and dysfunction noted in PE . Several studies also support an anti‐inflammatory/stabilizing function for HBCs . Cultures of HBCs released prostaglandin E 2 , supported trophoblast function, and suppressed T‐cell responses .…”

Section: Discussionmentioning

confidence: 99%

Decreased Levels of Folate Receptor‐β and Reduced Numbers of Fetal Macrophages (Hofbauer Cells) in Placentas from Pregnancies with Severe Pre‐Eclampsia

Tang

Buhimschi

et al. 2013

American J Rep Immunol

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“…Macrophages within the uteroplacental environment are an important source of bioactive mediators including prostaglandins and cytokines. Placental and decidual macrophages express COX-2 and produce PGE 2 in response to LPS or the pro-inflammatory cytokine IL-1β [ 25 – 29 ]. No studies to date have examined the effects of environmental toxicants, such as MEHP, on inducible COX-2 expression or prostaglandin secretion in macrophages from the utero-placental unit.…”

Section: Introductionmentioning

confidence: 99%

Mono-ethylhexyl phthalate stimulates prostaglandin secretion in human placental macrophages and THP-1 cells

Tetz

Aronoff

Loch‐Caruso

2015

Reprod Biol Endocrinol

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BackgroundDiethylhexyl phthalate (DEHP) is widely used as a plasticizer in polyvinyl chloride products. DEHP exposure, which is widespread in the US, increases preterm birth risk; however, the mechanisms driving this relationship are unclear. Because cyclooxygenase-2 (COX-2) dependent prostaglandin synthesis is implicated in preterm birth, we evaluated effects of mono-2-ethylhexyl phthalate (MEHP), the active metabolite of DEHP, on prostaglandin E2 (PGE2) synthesis and COX expression in human placental macrophages (PM). In addition, responses in PM were compared to those in a human macrophage-like cell line, THP-1.MethodsPM and THP-1 cells were treated for 2, 4, 8, or 24 h with MEHP concentrations ranging from 10 to 180 micromolar. PGE2 concentrations were assessed in culture medium using ELISA, and COX expression was determined by western blot.ResultsTreatment of PM and THP-1 cells with 180 micromolar MEHP for 24 h significantly increased PGE2 release. Co-treatment of PMs or THP-1 cells with 180 micromolar MEHP and the non-selective COX inhibitor indomethacin reduced MEHP-stimulated PGE2 production. Similarly, co-treatment of PM and THP-1 cells with the COX-2 selective inhibitor NS-398 resulted in a significant decrease in PGE2, suggesting that MEHP-stimulated PGE2 is dependent specifically on increased COX-2 expression. Western blot analysis revealed a significant increase in COX-2 expression in PM and THP-1 cells treated with 180 micromolar MEHP, and no changes in COX-1 expression, supporting the role of COX-2 in MEHP-stimulated PGE2 synthesis.ConclusionsThe findings from this study are the first to demonstrate phthalate-stimulated PGE2 synthesis in PM and warrant future studies into COX-2-dependent prostaglandin synthesis as a mechanism of toxicant-associated preterm birth.Electronic supplementary materialThe online version of this article (doi:10.1186/s12958-015-0046-8) contains supplementary material, which is available to authorized users.

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