PTX3 as a potential endothelial dysfunction biomarker for severity of preeclampsia and IUGR.
Endothelial dysfunction typical of preeclampsia (PE) is the result of an excessive maternal inflammatory response to pregnancy. We investigated PTX3 in maternal, fetal and placental compartments in complicated pregnancies. Maternal blood samples were collected during the third trimester in 53 PE, 43 IUGR (intrauterine growth restriction) and 50 normal pregnancies. Fetal samples were collected from the umbilical vein in 26 PE, 23 IUGR and 26 normal pregnancies at elective cesarean section. Pattern and site of expression of PTX3 were studied by immunohistochemistry (IHC) on placenta, decidual bed and maternal peritoneum. PE and IUGR pregnancies had significantly higher maternal PTX3 levels compared to normal pregnancies, with IUGR significantly lower than PE. Maternal peritoneum expressed a significantly higher signal in the endothelium of pathological compared to normal pregnancies. The maternal increase of PTX3 correlated with the severity of disease with higher PTX3 concentrations in severe PE. Increased PTX3 levels in PE and IUGR mothers, together with IHC data represent the expression of altered endothelial function on the maternal side. IUGR fetuses had higher PTX3 values than controls and the increase was related to IUGR severity, likely reflecting the hypoxic environment. These data confirm the relevance of PTX3 in support the hypothesis that PE is a disease associated with altered maternal endothelial function. The PTX3 increase in IUGR fetuses deserves further investigation.
Unit of Obstetrics and Gynecology and Center for Fetal Research Giorgio Pardi, Department of Biomedical and Clinical Sciences "L. Sacco", University of Milan, Via G.B. Grassi 74, 20151 Milano, Italy.
V
V
Cozzi
C
C
Garlanda
M
M
Nebuloni
V
V
Maina
A
A
Martinelli
S
S
Calabrese
I
I
Cetin
D000293:Adolescent; D000328:Adult; D015415:Biomarkers / Q000097:blood / Q000378:metabolism; D002097:C-Reactive Protein / Q000378:metabolism*; D003656:Decidua / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D004730:Endothelium, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D005260:Female; D005312:Fetal Blood; D005317:Fetal Growth Retardation / Q000097:blood* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D006801:Humans; D010537:Peritoneum / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D010920:Placenta / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D011225:Pre-Eclampsia / Q000097:blood* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011247:Pregnancy; D011263:Pregnancy Trimester, Third; D011446:Prospective Studies; D000683:Serum Amyloid P-Component / Q000378:metabolism*; D012720:Severity of Illness Index; D015854:Up-Regulation; D014652:Vascular Diseases / Q000209:etiology; D055815:Young Adult; D000099153:Pentraxins
D015415:Biomarkers; D002097:C-Reactive Protein; D000683:Serum Amyloid P-Component; D000099153:Pentraxins