Efeito da exposição pré-natal ao álcool na expressão de genes relacionados à hipertrofia cardíaca em camundongos C57Bl/6

• Ano de defesa: 2020
• Autor(a) principal: Atum, Allan Luís Barboza
• Orientador(a): Silva Junior, Jose Antonio
• Banca de defesa: Silva Junior, Jose Antonio , Dalboni, Maria Aparecida , Costa, Maricilia Silva
• Tipo de documento: Dissertação
• Tipo de acesso: Acesso aberto
• Idioma: por
• Instituição de defesa: Universidade Nove de Julho
• Programa de Pós-Graduação: Programa de Mestrado em Medicina
• Departamento: Saúde
• País: Brasil
• Palavras-chave em Português: exposição pré-natal ao álcool; expressão gênica; coração; transdução de sinal; prole
• Palavras-chave em Inglês: fetal alcohol exposure; gene expression; heart; signal transduction; offspring
• Área do conhecimento CNPq: CIENCIAS DA SAUDE
• Link de acesso: http://bibliotecatede.uninove.br/handle/tede/2728

The potential impact of prenatal alcohol exposure varies considerably between individuals, which can lead to systemic morphological and genetic changes. However, many of these changes occur at the cellular level, and may, throughout life, predispose the individual to chronic diseases. The impact on the cardiovascular system can result in changes such as cardiac hypertrophy and valve defects, as well as changes in the expression of genes related to cardiac homeostasis. Thus, using isogenic C57Bl/6 mice exposed to alcohol during pregnancy at a ratio of 10% (v / v) diluted in drinking water, we verified the expression of differentially expressed genes participating in the signal transduction pathways related to cardiac hypertrophy in the left ventricle (LV), using customized TaqMan® plates in RT-qPCR equipment. In addition to morphometric changes such as low birth weight, overweight in adulthood and mild hypertrophy of the heart and LV, we verified changes in the transcription of 18 of the 20 genes analyzed. Thus, in our experimental model, prenatal alcohol exposure induced morphometric changes and cardiac hypertrophy, as well as modulated the transcription of genes related to this cardiovascular condition. In addition, our data suggest that these changes are comparable to those seen in animals with experimental cardiac dysfunctions such as myocardial infarction.