Thesis (M.Sc.)--Chulalongkorn University, 2012

Cellular aging are divided to 2 groups, a replicative aging such as fibroblast and a non-replicative aging such as brain. Recently, hypomethylation in aging was reported. In aging cells of PBMC, hypomethylation of Alu and HERV-K was correlated to advancing age, while hypermethylation of L1 was found at specific age. In this study, we tested whether hypomethylation change gene expression in cellular and searched for genes that cause hypomethylation in replicative aging. We screened for expression profiles of cellular and demethylation to compare using statistical methods, Student’s t-test and Pearson Chi-square test. The results showed that hypomethylation altered gene expression significantly in replicative aging. Moreover, 82 hypomethylated genes related replicative aging were extracted and compared with 516 expression profiles of gene knockdown experiment. Depending on their property, significant genes could be divided to 2 groups. There were 16 genes represented anti-aging function and 12 genes represented aging function also. For functional analysis, these 28 genes encoded various proteins such as transcription factor, RNA-binding protein, histone modification enzyme and other cytoplasmic proteins which related to many cellular phenotypes and age-associated disease. Furthermore,it was found that function of 3 genes, ELAV1, HDAC1 and EZH2, correlate with DNA methylation implied that hypomethylation in replicative aging should be regulated by ELAV1, HDAC1 and EZH2.