RESUMO
Maternal post-traumatic stress disorder (PTSD) increases the risk of adverse neurodevelopmental outcomes in the child. Epigenetic alternations may play an essential role in the negative effects of PTSD. This study was aimed to investigate the possible epigenetic alterations of maternal PTSD, which underpins the developmental and behavioral impact. 24 pregnant Sprague-Dawley (SD) rats were randomly grouped into PTSD and control groups. Open-field tests (OFTs), elevated pull maze (EPM) assays, gene expression profile chip tests, and methylated DNA immunoprecipitation sequencing (MeDIP-Seq) were performed on the offsprings 30 days after birth. The results showed that PTSD offsprings had lower body weights and OFT scores than control offsprings. Enzyme-linked immunosorbent assays showed that serotonin receptor (5-HT) and dopamine levels were significantly lower in PTSD offsprings than in control offsprings. In contrast, corticosterone levels were higher in the PTSD group than in the control group. In a comparison of the PTSD group versus the control group, 4,160 significantly differentially methylated loci containing 30,657 CpGs were identified; 2,487 genes, including 13 dysmethylated genes, were validated by gene expression profiling, showing a negative correlation between methylation and gene expression (R = -0.617, P = 0.043). In conclusion, maternal PTSD could delay the physical and behavioral development of offsprings, and the underlying mechanism could contribute to changes in neurotransmitters and gene expression, owing to dysregulation of whole-genome methylation. These findings could support further clinical research on appropriate interventions for maternal PTSD to prevent methylation dysregulation and developmental retardation.
Assuntos
Deficiências do Desenvolvimento/metabolismo , Epigênese Genética , Efeitos Tardios da Exposição Pré-Natal/metabolismo , Transtornos de Estresse Pós-Traumáticos/complicações , Animais , Peso Corporal , Corticosterona/sangue , Metilação de DNA , Deficiências do Desenvolvimento/genética , Deficiências do Desenvolvimento/psicologia , Feminino , Gravidez , Efeitos Tardios da Exposição Pré-Natal/genética , Efeitos Tardios da Exposição Pré-Natal/psicologia , Ratos Sprague-Dawley , Transtornos de Estresse Pós-Traumáticos/genética , Transtornos de Estresse Pós-Traumáticos/metabolismo , Transcriptoma , Aumento de PesoRESUMO
Os autores apresentam um caso de feocromocitoma rastreado com metaiodobenzilguanidina marcada com 131I (MIBG-131I). Esta metodologia identifica a lesäo primitiva, sua recorrência e sua metastatizaçäo. Säo apontadas as vantagens do ensaio pela sua especificidade, sensibilidade e inoqüidade, oferecendo informaçöes ímpares de natureza morfofuncional no diagnóstico e acompanhamento evolutivo dessa doença