PMID- 12547721
OWN - NLM
STAT- MEDLINE
DCOM- 20030411
LR  - 20240408
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 162
IP  - 2
DP  - 2003 Feb
TI  - Differences in apoptotic susceptibility of cytotrophoblasts and 
      syncytiotrophoblasts in normal pregnancy to those complicated with preeclampsia 
      and intrauterine growth restriction.
PG  - 637-43
AB  - Placental apoptosis is increased in vivo in preeclampsia (PE) and intrauterine 
      growth restriction (IUGR). The cause and pathological implications of this 
      phenomenon are unknown. This study considers the apoptotic susceptibility of 
      villous trophoblasts from normal, PE, and IUGR pregnancies. Cultured 
      cytotrophoblasts (CTs) and an in vitro model of syncytialization were used. CTs 
      were isolated from term placentas of 12 normal, 12 PE, and 12 IUGR pregnancies. 
      Apoptosis was determined by terminal dUTP nick-end labeling (TUNEL), Annexin V 
      binding, and ADP:ATP ratios. Cells were stimulated with tumor necrosis 
      factor-alpha/interferon-gamma or reduced oxygen (<5 KPa). For CTs, ADP:ATP <1 
      correlates with Annexin V binding. For normal pregnancy, tumor necrosis 
      factor-alpha and depleted oxygen significantly increased TUNEL, Annexin V binding 
      and ADP:ATP in CTs and syncytiotrophoblasts (STs). Spontaneous apoptosis was 
      similar between groups for both cell types. After stimulation, TUNEL and Annexin 
      V binding of CTs were significantly raised in PE and IUGR as compared with normal 
      pregnancy. After oxygen reduction, ADP:ATP in CTs and STs were significantly 
      elevated in IUGR. TUNEL was also increased in STs in PE after oxygen depletion 
      and was significantly raised in STs from IUGR pregnancies after stimulation with 
      both agonists. This is the first description of enhanced apoptosis in isolated 
      villous trophoblasts in PE and IUGR. These intrinsic differences may represent an 
      important factor in the pathophysiology of these conditions.
FAU - Crocker, Ian P
AU  - Crocker IP
AD  - Maternal and Fetal Health Research Centre, University of Manchester, St. Mary's 
      Hospital, Manchester, UK. ian.crocker@man.ac.uk
FAU - Cooper, Suzanne
AU  - Cooper S
FAU - Ong, Stephen C
AU  - Ong SC
FAU - Baker, Philip N
AU  - Baker PN
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Annexin A5)
RN  - 0 (Chorionic Gonadotropin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 61D2G4IYVH (Adenosine Diphosphate)
RN  - 82115-62-6 (Interferon-gamma)
RN  - 8L70Q75FXE (Adenosine Triphosphate)
SB  - IM
MH  - Adenosine Diphosphate/metabolism
MH  - Adenosine Triphosphate/metabolism
MH  - Adult
MH  - Annexin A5/metabolism
MH  - *Apoptosis
MH  - Cells, Cultured
MH  - Chorionic Gonadotropin/analysis
MH  - Female
MH  - Fetal Growth Retardation/*pathology
MH  - Humans
MH  - In Situ Nick-End Labeling
MH  - Interferon-gamma/pharmacology
MH  - Maternal Age
MH  - Middle Aged
MH  - Models, Biological
MH  - Oxygen Consumption/drug effects
MH  - Parity
MH  - Pre-Eclampsia/*pathology
MH  - Pregnancy/*physiology
MH  - Trophoblasts/classification/*cytology/*pathology
MH  - Tumor Necrosis Factor-alpha/pharmacology
PMC - PMC1851173
EDAT- 2003/01/28 04:00
MHDA- 2003/04/12 05:00
PMCR- 2003/08/01
CRDT- 2003/01/28 04:00
PHST- 2003/01/28 04:00 [pubmed]
PHST- 2003/04/12 05:00 [medline]
PHST- 2003/01/28 04:00 [entrez]
PHST- 2003/08/01 00:00 [pmc-release]
AID - S0002-9440(10)63857-6 [pii]
AID - 3485 [pii]
AID - 10.1016/S0002-9440(10)63857-6 [doi]
PST - ppublish
SO  - Am J Pathol. 2003 Feb;162(2):637-43. doi: 10.1016/S0002-9440(10)63857-6.