| First Author | Poggi SH | Year | 2003 |
| Journal | Am J Obstet Gynecol | Volume | 189 |
| Issue | 3 | Pages | 786-9 |
| PubMed ID | 14526314 | Mgi Jnum | J:86352 |
| Mgi Id | MGI:2679469 | Doi | 10.1067/s0002-9378(03)00841-x |
| Citation | Poggi SH, et al. (2003) Differential expression of c-fos in a mouse model of fetal alcohol syndrome. Am J Obstet Gynecol 189(3):786-9 |
| abstractText | OBJECTIVE: Fetal alcohol syndrome (FAS) results in stillbirth, fetal growth restriction, and mental retardation with injury attributed to oxidative stress. Our objective was to identify signal transduction pathways expressed in a model of FAS and to quantify expression of c-fos, a gene in the stress signal pathway. STUDY DESIGN: Timed, pregnant C57Bl6/J mice were injected on E8 with saline solution or alcohol. RNA was extracted from decidua and embryo 6 and 24 hours later. Microarray analysis was used to screen gene pathways. Differential gene expression was confirmed using real-time polymerase chain reaction with results presented as the ratio of c-fos concentration to that of glyceraldehyde-3-phosphate dehydrogenase (GAPDH). RESULTS: Differential gene expression between alcohol and control was noted for stress signal pathway genes including c-fos. Real-time polymerase chain reaction demonstrated that c-fos messenger RNA expression was greater in the alcohol than control decidua at 6 hours after injection (P<.01). This effect persisted at 24 hours (P<.01). There was no difference in c-fos expression in embryos whose mothers received alcohol versus control after 6 hours (P=.12) or 24 hours (P=.89). CONCLUSION: Alcohol administration during pregnancy results in differential gene expression in the stress signal pathway, particularly in c-fos. C-fos expression in the decidua increases from 6 to 24 hours after alcohol injection, but does not change in the embryo, which may contribute to alcohol-induced damage in FAS. |
