Decreased expression of PAI-2 mRNA and protein in pregnancies complicated with intrauterine fetal growth retardation.
An increase in plasma plasminogen activator inhibitors (PAIs), fundamentally PAI type 2 (PAI-2), has been described in normal pregnancy probably because the placenta is the main source of the high plasma levels of this protein. Although we have previously described plasmatic alterations of these inhibitors in pregnancies complicated with intrauterine fetal growth retardation (IUGR), no reports have been published about placental PAI-2 mRNA expression. In the present study, the placental PAI-2 expression determined in pregnancies complicated with IUGR and in severe preeclamptic patients was compared with that of normal pregnancies in order to identify the placental cell types expressing PAI-2 and to determine whether the production of PAI-2 is altered in placentas from IUGR. In situ hybridization analyses show that the syncytiotrophoblasts are the cells with the greatest PAI-2 expression in placenta. We report that the significant decrease in plasma and placental PAI-2 levels in IUGR groups is fundamentally due to a diminished expression of PAI-2 mRNA in placenta.
Grancha
S
S
Research Center, Department of Pathology, La Fe Universitary Hospital, Valencia, Spain.
Estellés
A
A
Gilabert
J
J
Chirivella
M
M
España
F
F
Aznar
J
J
D000328:Adult; D005260:Female; D005317:Fetal Growth Retardation / Q000378:metabolism*; D005786:Gene Expression Regulation; D006801:Humans; D017403:In Situ Hybridization; D007231:Infant, Newborn; D010920:Placenta / Q000378:metabolism*; D017396:Plasminogen Activator Inhibitor 2 / Q000096:biosynthesis / Q000235:genetics*; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy / Q000097:blood*; D012333:RNA, Messenger / Q000096:biosynthesis* / Q000235:genetics
D017396:Plasminogen Activator Inhibitor 2; D012333:RNA, Messenger