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Published on: April 24, 2013
Vasoactive intestinal peptide mRNA and immunoreactivity are decreased in fetal alcohol syndrome model
Catherine Y Spong1, Jonathan Auth, Joy Vink
1Section on Developmental and Molecular Pharmacology, Laboratory of Developmental Neurobiology, NICHD, NIH, Building 49, Room 5A-38, MSC 4480, 9000 Rockville Pike, Bethesda, MD 20892, USA. spongc@exchange.nih.gov
Insights
Alcohol exposure decreases vasoactive intestinal peptide (VIP) levels in maternal and fetal tissues, potentially contributing to fetal alcohol syndrome. Peptide treatment may counteract these effects, preserving VIP regulation of embryonic development.
Area of Science:
- Developmental Biology
- Neuroendocrinology
- Toxicology
Background:
- Vasoactive intestinal peptide (VIP) is crucial for embryonic growth post-implantation.
- Previous studies showed VIP-regulated peptides mitigate alcohol-induced fetal alcohol syndrome (FAS) effects.
- The role of VIP itself in alcohol's impact on FAS requires further investigation.
Purpose of the Study:
- To investigate alterations in fetal and maternal VIP levels during alcohol exposure in a mouse model of FAS.
- To determine if peptide treatment can prevent alcohol-induced changes in VIP levels.
- To assess the impact of alcohol on VIP gene expression.
Main Methods:
- Enzyme immunoassay (EIA) for VIP quantification.
- Reverse transcription-polymerase chain reaction (rt-PCR) for VIP mRNA expression analysis.
- Treatment groups: control, alcohol, and alcohol+peptides.
Main Results:
- Alcohol significantly reduced VIP levels in embryo/deciduas at 12 and 24 hours post-exposure.
- Maternal cortex VIP levels were significantly lower in alcohol-treated mice.
- Alcohol exposure decreased VIP mRNA expression in embryo/deciduas, an effect attenuated by peptide pretreatment.
Conclusions:
- Alcohol exposure diminishes both the expression and immunoreactivity of VIP in maternal and fetal tissues.
- Reduced VIP, a key regulator of embryonic development, may underlie alcohol's teratogenic effects in FAS.
- Peptide agonists show potential in mitigating alcohol's adverse effects on VIP signaling during pregnancy.
Abstract:
Vasoactive intestinal peptide (VIP) regulates growth in the early post-implantation embryo. Previous work has demonstrated that peptide agonists (SALLRSIPA and NAPVSIPQ) from downstream mediators that are regulated by VIP were able to prevent the alcohol-induced fetal death, growth restriction and microcephaly associated with fetal alcohol syndrome. Here we evaluated the role of VIP in this mouse model of fetal alcohol syndrome, to determine if fetal or maternal levels of VIP are altered. In addition, we evaluated whether peptide treatment would alter the effects of alcohol on VIP levels. Treatment groups included control, alcohol, and alcohol+peptides. VIP levels were measured with enzyme immunoassay [EIA] (Peninsula Laboratories, Belmont, CA). Quantitation of VIP expression was measured with rt-PCR using mimic cDNA primers. Embryo/decidual VIP levels were similar in control and alcohol-treated groups 6 h after treatment. However, in the embryo/deciduas at 12 and 24 h, VIP levels were below the EIA's detection limit in the alcohol-treated groups, and significantly lower than the control or peptide-pretreated groups (p<0.05). Maternal cortex VIP levels were undetectable and significantly lower in the alcohol-treated group than control or peptide+alcohol group at 6 and 12 h (p<0.001). VIP mRNA expression was quantitated in the embryo and deciduas, with a significant decline noted at 6 h to 58% of control levels (p=0.02). Pretreatment with the peptides attenuated the alcohol-induced decrease in VIP mRNA. These studies demonstrate that treatment with alcohol can decrease the expression and immunoreactivity of VIP in both maternal and fetal tissues. This alcohol-induced loss of a recognized regulator of embryonic growth and differentiation may contribute to the sequelae of toxicity observed in fetal alcohol syndrome.
