Methylation profile, genomic instability and gene expression evaluations related with cardiovascular diseases in mice supplemented with methionine diet

• Grant number: 13/02365-6
• Support Opportunities: Regular Research Grants
• Start date: July 01, 2013
• End date: July 31, 2015
• Field of knowledge: Health Sciences - Nutrition - Nutrition Biochemistry
• Principal Investigator: Lusânia Maria Greggi Antunes
• Grantee: Lusânia Maria Greggi Antunes
• Host Institution: Faculdade de Ciências Farmacêuticas de Ribeirão Preto (FCFRP). Universidade de São Paulo (USP). Ribeirão Preto , SP, Brazil

Abstract

Nutritional deficiency during the embryonic period is a health problem in many populations. It is known that the lack of nutrients in pregnancy is one of the mechanisms that can influence the health of both mother and newborn. During the reproductive process, the genome of mammals undergoes a profound reprogramming of methylation patterns in germ cells and in the early stages of pre-implantation embryo. Some of bioactive nutrients, such as methionine, choline, folic acid, vitamins B6 and B12, can modulate DNA methylation in mammals. Alterations that arise during the embryonic period may still induce the onset of diseases throughout the adult life of the individual. Studies suggest that one of the mechanisms that are most influenced by the diet in this period is the process of DNA methylation. It is also well known that problems in DNA methylation affect the gene expression and genomic stability, which are linked to the risk of cardiovascular disease. Therefore, this study could help to understand how genes that have CpG islands in its promoter regions, could be expressed in animals, during the pregnancy, fed a diet with different concentrations of methionine, the most important donor of methyl group. There will also be evaluated the effects of diets supplemented or deficient in methionine on epigenetic alterations of DNA, gene expression, genomic instability and biochemical markers in female mice after pregnancy, as well as their offspring. (AU)

Scientific publications

(4)

(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)

AISSA, ALEXANDRE FERRO; DO AMARAL, CATIA LIRA; VENANCIO, VINICIUS PAULA; MACHADO, CARLA DA SILVA; HERNANDES, LIVIA CRISTINA; DA SILVA SANTOS, PATRICK WELLINGTON; CURI, RUI; PIRES BIANCHI, MARIA DE LOURDES; GREGGI ANTUNES, LUSANIA MARIA. Methionine-supplemented diet affects the expression of cardiovascular disease-related genes and increases inflammatory cytokines in mice heart and liver. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 80, n. 19-21, SI, p. 1116-1128, 2017. (13/02365-6, 10/01410-0)

AISSA, ALEXANDRE FERRO; TRYNDYAK, VOLODYMYR P.; DE CONTI, ALINE; THOMAZELA MACHADO, ANA RITA; TUTTIS, KATIUSKA; MACHADO, CARLA DA SILVA; HERNANDES, LIVIA CRISTINA; DA SILVA SANTOS, PATRICK WELLINGTON; SERPELONI, JULIANA MARA; POGRIBNY, IGOR P.; et al. Epigenetic changes induced in mice liver by methionine-supplemented and methionine-deficient diets. Food and Chemical Toxicology, v. 163, p. 10-pg., 2022-05-01. (10/01410-0, 13/02365-6)

AISSA, ALEXANDRE FERRO; URSULA HERMOGENES GOMES, TARSILA DAYSY; ALMEIDA, MARA RIBEIRO; HERNANDES, LIVIA CRISTINA; CASTANIA DARIN, JOANA D'ARC; PIRES BIANCHI, MARIA LOURDES; GREGGI ANTUNES, LUSANIA MARIA. Methionine concentration in the diet has a tissue-specific effect on chromosomal stability in female mice. Food and Chemical Toxicology, v. 62, p. 456-462, DEC 2013. (13/02365-6, 10/01410-0)

AISSA, ALEXANDRE FERRO; DO AMARAL, CATIA LIRA; VENANCIO, VINICIUS PAULA; MACHADO, CARLA DA SILVA; HERNANDES, LIVIA CRISTINA; DA SILVA SANTOS, PATRICK WELLINGTON; CURI, RUI; PIRES BIANCHI, MARIA DE LOURDES; GREGGI ANTUNES, LUSANIA MARIA. Methionine-supplemented diet affects the expression of cardiovascular disease-related genes and increases inflammatory cytokines in mice heart and liver. JOURNAL OF TOXICOLOGY AND ENVIRONMENTAL HEALTH-PART A-CURRENT ISSUES, v. 80, n. 19-21, p. 13-pg., 2017-01-01. (13/02365-6, 10/01410-0)