title: Heme oxygenase expression in human placenta and placental bed: reduced expression of placenta endothelial HO-2 in preeclampsia and fetal growth restriction.
abstract: In this study we tested the hypothesis that expression of heme oxygenases HO-1 and HO-2, which are responsible for the production of carbon monoxide, are reduced in the placenta and placental bed of pregnancies complicated by preeclampsia (PE) and fetal growth restriction (FGR) compared with control third-trimester pregnancies. Placental protein expression was determined by Western blotting (n=10 in each group) and immunohistochemistry (controls n=18, PE n=19, FGR n=10). Extravillous trophoblast expression was determined by immunohistochemistry of placental bed biopsy samples (controls n=17, PE n=19, FGR n=10). Western blot analysis of placental homogenates showed no overall differences in HO-2 among groups. However, immunohistochemical analysis showed a reduction in HO-2 expression in endothelial cells in both abnormal groups (PE P<0.01; FGR P<0.0005 vs. control group) but no differences in villous trophoblast staining. HO-1 was undetectable by Western blotting in control and abnormal pregnancies and immunoreactivity was very low, suggesting that there is little HO-1 in the placenta. Within the placental bed, HO-2 but not HO-1 was detected on all populations of extravillous trophoblast, but expression of HO-2 or HO-1 did not change in PE or FGR. The reduced expression of HO-2 on endothelial cells in PE and FGR may be responsible for reduced placental blood flow in these conditions. The data do not show changes in HO in the placental bed in PE or FGR.
authors.affiliation: Maternal and Fetal Medicine Section, Institute of Medical Genetics, Yorkhill, Glasgow G3 8SJ, UK.
authors.forename: A
authors.initials: A
authors.lastname: Barber
authors.forename: S C
authors.initials: SC
authors.lastname: Robson
authors.forename: L
authors.initials: L
authors.lastname: Myatt
authors.forename: J N
authors.initials: JN
authors.lastname: Bulmer
authors.forename: F
authors.initials: F
authors.lastname: Lyall
mesh_terms: D000328:Adult; D001706:Biopsy; D015153:Blotting, Western; D016022:Case-Control Studies; D004727:Endothelium / Q000166:cytology / Q000201:enzymology; D005260:Female; D005317:Fetal Growth Retardation / Q000201:enzymology* / Q000503:physiopathology; D005333:Fetus / Q000502:physiology; D006419:Heme Oxygenase (Decyclizing) / Q000378:metabolism*; D051547:Heme Oxygenase-1; D006801:Humans; D007150:Immunohistochemistry; D007633:Keratins / Q000378:metabolism; D008565:Membrane Proteins; D010920:Placenta / Q000098:blood supply / Q000166:cytology / Q000201:enzymology*; D011225:Pre-Eclampsia / Q000201:enzymology* / Q000503:physiopathology; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D020033:Protein Isoforms / Q000378:metabolism
chemical_list: D008565:Membrane Proteins; D020033:Protein Isoforms; D007633:Keratins; C496541:HMOX1 protein, human; D006419:Heme Oxygenase (Decyclizing); D051547:Heme Oxygenase-1; C105245:heme oxygenase-2