This work was supported in part by a McKern Scholar Award for Perinatal Research (SG) and P01 Grant HD054713-01 (SG) from the NIH.
Decreased Levels of Folate Receptor-β and Reduced Numbers of Fetal Macrophages (Hofbauer Cells) in Placentas from Pregnancies with Severe Pre-Eclampsia†
Version of Record online: 11 MAR 2013
© 2013 John Wiley & Sons A/S
American Journal of Reproductive Immunology
Volume 70, Issue 2, pages 104–115, August 2013
How to Cite
Decreased levels of folate receptor-β and reduced numbers of fetal macrophages (Hofbauer cells) in placentas from pregnancies with severe pre-eclampsia. Am J Reprod Immunol 2013; 70: 104–115, , , , , , , .
- Issue online: 10 JUL 2013
- Version of Record online: 11 MAR 2013
- Manuscript Accepted: 11 FEB 2013
- Manuscript Received: 8 JAN 2013
- fetal macrophages;
- folate receptor;
- Hofbauer cells;
Pre-eclampsia (PE), a pregnancy complication of unknown etiology, is a major cause of maternal and fetal mortality and morbidity. Previous studies have described placental genes that 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 with 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.
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 with the sPTB group. Numbers of Hofbauer cells (HBCs, fetal macrophages) and FR-β protein in these cells were reduced in PE group placentas.
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.