Document Detail


The role of activity-dependent neuroprotective protein in a mouse model of fetal alcohol syndrome.
MedLine Citation:
PMID:  14526315     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
OBJECTIVE: Fetal alcohol syndrome (FAS) is the most common nongenetic cause of mental retardation. Peptides NAPVSIPQ (NAP) and SALLRSIPA (SAL), related to activity-dependent neuroprotective protein (ADNP), prevent alcohol-induced damage in a mouse model of FAS. Our objective was to characterize ADNP in this model to relate this protein to the mechanisms of damage and peptide neuroprotection. STUDY DESIGN: Timed, pregnant C57Bl6/J mice were treated on day 8. Groups were control, alcohol, peptide pretreatment, or peptide alone. Embryo and decidua were harvested at 6 and 24 hours and 10 days. To evaluate ADNP expression, real-time polymerase chain reaction was performed with results presented as the ratio of ADNP-to-glyceraldehyde-3-phosphate dehydrogenase (GAPDH) concentration. Analysis of variance was performed for overall comparisons with P<.05 considered significant. RESULTS: At 6 hours, there was no difference in ADNP between alcohol-exposed embryos compared with control embryos. At 24 hours, there was an increase in ADNP in alcohol-exposed embryos compared with controls (P<.001); these findings persisted at 10 days (P<.001). In the decidua at 6 hours, there was no difference between alcohol and control. At 24 hours, there was greater ADNP in alcohol-exposed decidua compared with controls (P<.001), which did not persist at 10 days (P=.97). Peptide pretreatment did not prevent the alcohol-induced increase in ADNP in embryo or decidua. CONCLUSION: Alcohol increased embryonic and decidual ADNP expression at 24 hours and it persisted in the embryo for 10 days. Because ADNP is a known neuroprotectant, these findings suggest that it may be released as a protective mechanism in FAS. Changes in the embryo were persistent suggesting that the embryo is more vulnerable to alcohol-induced damage than the mother.
Authors:
Sarah H Poggi; Katie Goodwin; Joanna M Hill; Douglas E Brenneman; Elizabetta Tendi; Sergio Schinelli; Daniel Abebe; Catherine Y Spong
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  American journal of obstetrics and gynecology     Volume:  189     ISSN:  0002-9378     ISO Abbreviation:  Am. J. Obstet. Gynecol.     Publication Date:  2003 Sep 
Date Detail:
Created Date:  2003-10-03     Completed Date:  2003-11-04     Revised Date:  2007-11-15    
Medline Journal Info:
Nlm Unique ID:  0370476     Medline TA:  Am J Obstet Gynecol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  790-3     Citation Subset:  AIM; IM    
Affiliation:
Department of Obstetrics and Gynecology, Georgetown University Hospital, Washington, DC, USA. shp2@gunet.georgetown.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Decidua / chemistry
Disease Models, Animal*
Embryo, Mammalian / chemistry
Ethanol / administration & dosage
Female
Fetal Alcohol Syndrome / physiopathology*
Gene Expression
Glyceraldehyde-3-Phosphate Dehydrogenases / genetics
Homeodomain Proteins / administration & dosage,  genetics,  physiology*
Mice
Mice, Inbred C57BL
Nerve Tissue Proteins / administration & dosage,  genetics,  physiology*
Pregnancy
RNA, Messenger / analysis
Reverse Transcriptase Polymerase Chain Reaction
Chemical
Reg. No./Substance:
0/Adnp protein, mouse; 0/Homeodomain Proteins; 0/Nerve Tissue Proteins; 0/RNA, Messenger; 64-17-5/Ethanol; EC 1.2.1.-/Glyceraldehyde-3-Phosphate Dehydrogenases

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