PMID- 19114963
OWN - NLM
STAT- MEDLINE
DCOM- 20090316
LR  - 20201209
IS  - 1643-3750 (Electronic)
IS  - 1234-1010 (Linking)
VI  - 15
IP  - 1
DP  - 2009 Jan
TI  - Ethanol inhibited apoptosis-related RNA binding protein, Napor-3 gene expression 
      in the prenatal rat brain.
PG  - BR6-12
AB  - BACKGROUND: Cell death and differentiations are the critical processes in 
      developing fetal brain, where ethanol induces lots of changes in gene expression 
      patterns of fetal nervous system leading to fetal alcohol syndrome (FAS). The 
      objective of the present study was to observe whether maternal ethanol exposure 
      can alter gene expression pattern in mother and in fetus during mid and late 
      prenatal stage. MATERIAL/METHODS: 10% ethanol was orally applied to female 
      Spraque-Dawley rats and fetuses were sacrificed on gestational day (GD) 19.5 and 
      21.5. Total mRNA was isolated for differential-display PCR (DD-PCR) and sequence 
      was analyzed to find out the homologous gene(s) using GenBank database of the 
      BLAST program. Finally, the gene expression pattern in different maternal and 
      fetal brain areas of the control and the ethanol treated groups were studied by 
      RNase protection assay (RPA) and in situ hybridization. RESULTS: Out of several 
      differentially expressed genes, apoptosis-related RNA binding protein (RBP), 
      'Napor-3' mRNA expression was significantly inhibited by ethanol in fetal rat 
      fore-, mid- and hind- brain, and adult rat cortex and hippocampus when compared 
      with the untreated control. The cDNA analysis was further supported our result 
      (accession: AF090697, 95% sequence homology). CONCLUSIONS: The age and area 
      dependent suppression of apoptosis-related RBP, Napor-3 gene expression in 
      proliferating fetal brain by maternal ethanol suggesting high susceptibility 
      towards ethanol intake at the time of neuronal cell development and 
      proliferation. Further, ethanol also affects maternal brain tissues that may be 
      one of the reasons for ethanol-induce irreversible damage of the developing 
      brain. The present study for the first time provides the evidence that Napor-3 
      suppression by ethanol during mid and late stage fetal brain converts natural 
      physiological event apoptosis into pathological process, which may be useful as a 
      novel therapeutic approach towards FAS-associated developmental brain damage as a 
      consequence of maternal drinking behavior.
FAU - Naha, Nibedita
AU  - Naha N
AD  - Division of Life Science, Applied Life Science (BK 21), College of Natural 
      Science, Gyeongsang National University, Jinju, South Korea.
FAU - Lee, Hae Young
AU  - Lee HY
FAU - Naser, Mohammad Imran
AU  - Naser MI
FAU - Park, Tae Ju
AU  - Park TJ
FAU - Kim, Sung Hoon
AU  - Kim SH
FAU - Kim, Myeong Ok
AU  - Kim MO
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Med Sci Monit
JT  - Medical science monitor : international medical journal of experimental and 
      clinical research
JID - 9609063
RN  - 0 (CELF Proteins)
RN  - 0 (Celf2 protein, rat)
RN  - 0 (DNA, Complementary)
RN  - 0 (Nerve Tissue Proteins)
RN  - 0 (RNA-Binding Proteins)
RN  - 3K9958V90M (Ethanol)
SB  - IM
MH  - Analysis of Variance
MH  - Animals
MH  - Apoptosis/*drug effects
MH  - Base Sequence
MH  - Brain/*drug effects/embryology/*metabolism
MH  - CELF Proteins
MH  - DNA, Complementary/genetics
MH  - Ethanol/*toxicity
MH  - Female
MH  - Gene Expression Regulation, Developmental/*drug effects
MH  - In Situ Hybridization
MH  - Male
MH  - Maternal Exposure/*adverse effects
MH  - Molecular Sequence Data
MH  - Nerve Tissue Proteins/genetics/*metabolism
MH  - RNA-Binding Proteins/genetics/*metabolism
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Sequence Analysis, DNA
EDAT- 2008/12/31 09:00
MHDA- 2009/03/17 09:00
CRDT- 2008/12/31 09:00
PHST- 2008/12/31 09:00 [entrez]
PHST- 2008/12/31 09:00 [pubmed]
PHST- 2009/03/17 09:00 [medline]
AID - 869518 [pii]
PST - ppublish
SO  - Med Sci Monit. 2009 Jan;15(1):BR6-12.