| The role of activity-dependent neuroprotective protein in a mouse model of fetal alcohol syndrome. | |
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MedLine Citation:
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PMID: 14526315 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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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:
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Type: Journal Article |
Journal Detail:
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Title: American journal of obstetrics and gynecology Volume: 189 ISSN: 0002-9378 ISO Abbreviation: Am. J. Obstet. Gynecol. Publication Date: 2003 Sep |
Date Detail:
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Created Date: 2003-10-03 Completed Date: 2003-11-04 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0370476 Medline TA: Am J Obstet Gynecol Country: United States |
Other Details:
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Languages: eng Pagination: 790-3 Citation Subset: AIM; IM |
Affiliation:
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Department of Obstetrics and Gynecology, Georgetown University Hospital, Washington, DC, USA. shp2@gunet.georgetown.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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