PMID- 19616844
OWN - NLM
STAT- MEDLINE
DCOM- 20091215
LR  - 20171116
IS  - 1532-3102 (Electronic)
IS  - 0143-4004 (Linking)
VI  - 30
IP  - 9
DP  - 2009 Sep
TI  - Increased placental apoptosis in maternal food restricted gestations: role of the 
      Fas pathway.
PG  - 739-51
LID - 10.1016/j.placenta.2009.06.003 [doi]
AB  - The placenta has a pivotal role, shuttling nutrients to the developing fetus and 
      producing hormones essential to pregnancy. Maternal food restriction (MFR) during 
      pregnancy results in growth restricted newborns, a consequence attributed 
      primarily to maternal nutrient supply. We hypothesized that MFR further 
      compromises fetal growth by decreased placental growth or increased placental 
      apoptosis. We determined the potential pathway (Fas-Fas-ligand; Fas-FasL) of 
      placental apoptosis in MFR pregnancies. We assessed the two morphologically and 
      functionally distinct zones (basal and labyrinth) at embryonic age 20 (E20) in ad 
      libitum fed controls (AdLib) and 50% MFR placentas. We studied fetuses and 
      placentas from both proximal and mid-horn positions to evaluate any differential 
      impact by MFR. Placenta apoptosis was quantified using terminal dUTP nick-end 
      labeling (TUNEL) assay and the data were compared to immunodetection of cleaved 
      caspase-3, Fas and FasL followed by Western blot quantification of Fas, FasL, 
      caspase-8 and -3, tBID, and poly-ADP-ribose polymerase (PARP). MFR reduced 
      maternal, fetal and placental basal and labyrinth weights. The results suggest 
      that the increased apoptosis may be mediated, in part, via Fas pathway and the 
      defective placental development in the MFR may be a major contributor to the 
      decreased fetal growth.
FAU - Belkacemi, L
AU  - Belkacemi L
AD  - LABioMed Research Institute at Harbor-UCLA Medical Center, Los Angeles, CA 90502, 
      USA. lbelkacemi@obgyn.humc.edu
FAU - Chen, C H
AU  - Chen CH
FAU - Ross, M G
AU  - Ross MG
FAU - Desai, M
AU  - Desai M
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20090718
PL  - Netherlands
TA  - Placenta
JT  - Placenta
JID - 8006349
RN  - 0 (BH3 Interacting Domain Death Agonist Protein)
RN  - 0 (Fas Ligand Protein)
RN  - 0 (fas Receptor)
RN  - EC 2.4.2.30 (Poly(ADP-ribose) Polymerases)
RN  - EC 3.4.22.- (Caspase 3)
RN  - EC 3.4.22.- (Caspase 8)
SB  - IM
MH  - Animals
MH  - *Apoptosis
MH  - BH3 Interacting Domain Death Agonist Protein/metabolism
MH  - Body Weight
MH  - Caspase 3/metabolism
MH  - Caspase 8/metabolism
MH  - Enzyme Activation
MH  - Fas Ligand Protein/metabolism
MH  - Female
MH  - Fetal Growth Retardation/etiology
MH  - Fetal Weight
MH  - Food Deprivation/*physiology
MH  - In Situ Nick-End Labeling
MH  - Male
MH  - Maternal-Fetal Exchange/physiology
MH  - Organ Size
MH  - Placenta/pathology/*physiology
MH  - Poly(ADP-ribose) Polymerases/metabolism
MH  - Pregnancy
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - *Signal Transduction
MH  - fas Receptor/*metabolism
EDAT- 2009/07/21 09:00
MHDA- 2009/12/16 06:00
CRDT- 2009/07/21 09:00
PHST- 2008/12/02 00:00 [received]
PHST- 2009/06/10 00:00 [revised]
PHST- 2009/06/16 00:00 [accepted]
PHST- 2009/07/21 09:00 [entrez]
PHST- 2009/07/21 09:00 [pubmed]
PHST- 2009/12/16 06:00 [medline]
AID - S0143-4004(09)00202-1 [pii]
AID - 10.1016/j.placenta.2009.06.003 [doi]
PST - ppublish
SO  - Placenta. 2009 Sep;30(9):739-51. doi: 10.1016/j.placenta.2009.06.003. Epub 2009 
      Jul 18.