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Quantitative abnormalities of fetal trophoblast cells in maternal circulation in preeclampsia
Author(s) -
Zhang Ling,
Wang Yan,
Liao AiHua
Publication year - 2008
Publication title -
prenatal diagnosis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.956
H-Index - 97
eISSN - 1097-0223
pISSN - 0197-3851
DOI - 10.1002/pd.2135
Subject(s) - trophoblast , testis determining factor , preeclampsia , fetus , andrology , y chromosome , biology , polymerase chain reaction , cell free fetal dna , microbiology and biotechnology , pregnancy , medicine , placenta , prenatal diagnosis , gene , genetics
Abstract Objective To determine if quantitative abnormalities of circulating fetal trophoblast cells (CFTCs) are associated with preeclampsia. Methods The trophoblast cell‐specific antibody, MEM‐G/9 (monoclonal antibody to HLA‐G), was applied to distinguish the trophoblast cells from the maternal circulation. The trophoblast cells were isolated by density‐gradient centrifugation from maternal blood samples of normal pregnant and preeclamptic women, respectively. After preliminary enrichment, the CFTCs were identified by immunocytochemical staining with the MEM‐G/9. To prove fetal origin of the HLA‐G‐positive cells, primer‐extension preamplification (PEP) and polymerase chain reaction (PCR) based on single HLA‐G‐positive cells were adopted to detect human sex‐determining region of the Y‐chromosome (SRY) gene. Results There were 6.88 ± 1.54 and 30.56 ± 5.16 HLA‐G‐positive cells in 6 mL maternal blood from the normal pregnant (n = 16) and preeclamptic women (n = 18), respectively. The difference was statistically significant ( p < 0.001). The SRY gene from the HLA‐G‐positive cells was detected in all pregnant women carrying male fetuses. The sensitivity and specificity of PEP and PCR for the SRY gene detection were 100%. Conclusion It is concluded that enhancement of CFTCs numbers is related to preeclampsia, which provides information useful for noninvasive prenatal diagnosis of preeclampsia. Copyright © 2008 John Wiley & Sons, Ltd.