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Markers of susceptibility to air pollution

Abstract

Epigenetic changes alters the pattern of gene expression without modifying the DNA sequence, and the its three most important mechanisms are DNA methylation, histones methylation/acetylation and microRNA silencing. Inflammation is a complex physiological response of an organism to noxious stimuli. Chronic inflammation is an underling cause for cardiovascular and pulmonary diseases and diabetes. Ambient air pollutants cause disruption of homeostasia of organisms exposed to them, generating cellular oxidative stress and setting inflammation. The objective of this study is to identify differences in the methylation pattern on the TNFL (inflammatory) and IL-10 (anti-inflammatory) cytokines genes promoter regions among individuals already identified as susceptible or not to pollution regarding to the inflammatory response. The DNA database to be used comes from a group of specialized workers in São Paulo city: CET traffic controllers, taxi drivers and professionals of Forestry Institute. The individual load of PM2,5 was measured for 24 hours in 4 occasions apart by a week. On the same occasions, all subjects underwent clinical and laboratory examinations at the HCFMUSP. The measurement of methylation pattern in the selected genes promoters will be done by pyrosequencing after cytosine derivatization by sodium bisulfite. (AU)

Articles published in Agência FAPESP Newsletter about the research grant:
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VEICULO: TITULO (DATA)
VEICULO: TITULO (DATA)

Scientific publications
(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)
MATSUDA, MONIQUE; BONATTI, RODOLFO; MARQUEZINI, MONICA V.; GARCIA, MARIA L. B.; SANTOS, UBIRATAN P.; BRAGA, ALFESIO L. F.; ALVES, MILTON R.; SALDIVA, PAULO H. N.; MONTEIRO, MARIO L. R.. Lacrimal Cytokines Assessment in Subjects Exposed to Different Levels of Ambient Air Pollution in a Large Metropolitan Area. PLoS One, v. 10, n. 11, . (14/50110-0)