PMID- 12478636
OWN - NLM
STAT- MEDLINE
DCOM- 20030603
LR  - 20171116
IS  - 0197-3851 (Print)
IS  - 0197-3851 (Linking)
VI  - 22
IP  - 13
DP  - 2002 Dec
TI  - Limited expression of Fas and Fas ligand in fetal nucleated erythrocytes isolated 
      from first trimester maternal blood.
PG  - 1213-8
AB  - OBJECTIVE: Intact fetal cells isolated from maternal blood can be used for 
      non-invasive gender determination and genetic diagnosis. Recent studies 
      demonstrating a large amount of cell-free fetal DNA in maternal plasma suggest 
      that the circulating fetal DNA may result from fetal cells undergoing apoptosis. 
      In the present study we evaluated the potential role of Fas and Fas ligand (FasL) 
      cell surface expression with respect to apoptosis induction in fetal cells 
      isolated from maternal blood. METHODS: We flow sorted candidate fetal cells that 
      were gamma chain-positive and Fas- or FasL-positive or -negative, and 
      subsequently analysed them by fluorescence in situ hybridization (FISH) analysis 
      using X and Y chromosome-specific probes. RESULTS: Among all gamma 
      hemoglobin-positive cells, there was a significant difference in the percent of 
      cells expressing Fas versus FasL (4.4 and 12.3, respectively). We found no 
      significant correlation between the total number of fetal nucleated red blood 
      cells (NRBCs) and gestational age or the presence of Fas- and FasL-positive 
      cells. From approximately 7 ml of maternal peripheral blood, most of the 
      confirmed fetal (XY) cells were found in the Fas- and FasL-negative sorted 
      population; the average numbers were 12.8 and 15.7, respectively. CONCLUSION: We 
      conclude that fetal NRBCs express FasL more than Fas, although most fetal NRBCs 
      in first trimester maternal blood samples do not express Fas or FasL. This 
      suggests the absence of a functional Fas/FasL apoptotic system in fetal NRBCs, 
      and that programmed cell death in these cells, which may lead to circulating 
      fetal DNA in maternal plasma, probably occurs by another pathway.
CI  - Copyright 2002 John Wiley & Sons, Ltd.
FAU - Sohda, Satoshi
AU  - Sohda S
AD  - Division of Genetics, Department of Pediatrics, New England Medical Center, Tufts 
      University School of Medicine, Boston, MA 02111, USA.
FAU - Samura, Osamu
AU  - Samura O
FAU - Johnson, Kirby L
AU  - Johnson KL
FAU - Falco, Vincent M
AU  - Falco VM
FAU - Elmes, R Sarah
AU  - Elmes RS
FAU - Bianchi, Diana W
AU  - Bianchi DW
LA  - eng
GR  - N01-HD-4-3204/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - England
TA  - Prenat Diagn
JT  - Prenatal diagnosis
JID - 8106540
RN  - 0 (FASLG protein, human)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (Membrane Glycoproteins)
RN  - 0 (fas Receptor)
RN  - 9007-49-2 (DNA)
SB  - IM
MH  - Adult
MH  - Apoptosis/physiology
MH  - DNA/analysis
MH  - DNA Fragmentation
MH  - Erythroblasts/*metabolism
MH  - Fas Ligand Protein
MH  - Female
MH  - Fetal Blood/*cytology/metabolism
MH  - Fetomaternal Transfusion
MH  - Flow Cytometry
MH  - Humans
MH  - In Situ Hybridization, Fluorescence
MH  - Membrane Glycoproteins/*metabolism
MH  - Pregnancy/*blood
MH  - Pregnancy Trimester, First
MH  - fas Receptor/*metabolism
EDAT- 2002/12/13 04:00
MHDA- 2003/06/05 05:00
CRDT- 2002/12/13 04:00
PHST- 2002/12/13 04:00 [pubmed]
PHST- 2003/06/05 05:00 [medline]
PHST- 2002/12/13 04:00 [entrez]
AID - 10.1002/pd.480 [doi]
PST - ppublish
SO  - Prenat Diagn. 2002 Dec;22(13):1213-8. doi: 10.1002/pd.480.