Expression of the nonclassic histocompatibility antigen HLA-G by preeclamptic placenta

Expression of the histocompatibility antigen HLA-G may be required for appropriate invasion and remodeling of uterine spiral arteries. Inappropriate expression of this antigen may result in failure of invasion, leading to partial placental ischemia and gestational disease.

To test the hypothesis that the level of expression of HLA-G is reduced in trophoblasts from patients with gestational complications (preeclampsia, intrauterine growth retardation, or gestational hypertension) compared with patients with normal pregnancy, total ribonucleic acid was isolated from the fetal membrane or decidual interface of term placenta from several patient groups. Ribonuclease protection assay was used to determine levels of HLA-G expression, which was normalized for total ribonucleic acid input with beta-actin and for trophoblast content in the tissue by cytokeratin 8.

When normalized for total ribonucleic acid input (beta-actin), term placental expression of HLA-G was reduced for all forms of preeclampsia but not for intrauterine growth retardation or gestational hypertension. When tissue expression of cytokeratin, an indicator of trophoblast input, was normalized for trophoblast input, was normalized for total ribonucleic acid input, primary preeclampsia and intrauterine growth retardation had reduced numbers of trophoblast per unit tissue. When controlled for trophoblast input HLA-G expression was similar to normal for all clinical groups, except for intrauterine growth retardation, which was slightly increased.

Level of expression of HLA-G in placental tissue was reduced in preeclampsia. This decrease in expression appears to be related to reduced numbers of trophoblasts in placental tissue examined at term from patients with primary preeclampsia.