The role of p16 methylation in the aging of human fetal lung diploid fibroblasts
- VernacularTitle:p16基因甲基化在人二倍体成纤维细胞衰老中的作用
- Author:
Peili CHEN
;
Tanjun TONG
;
Zongyu ZHANG
- Publication Type:Journal Article
- From:
Chinese Journal of Geriatrics
2001;20(1):44-46
- CountryChina
- Language:Chinese
-
Abstract:
Objective The relationship between DNA methylation and the overexpression of cell cycle negative regulator p16MTS1/INK4a in senescent cells was studied. Methods PCR amplification of p16 exon I following digestion with Sma I , a methylation sensitive DNA endonuclease, was adapted to determine the methylation status at specific site. Results T-he increased expression of p16 in the aging process of human fetal lung diploid fibroblasts (2BS) was observed. In middle-aged and old cells, the p16 level was about 3 folds and 10 folds respectively as that in young cells. The methylation level of the Sma I site in p16 exon I tended to decline with aging, being about 64% and 41% in young and middle-aged cells respectively, but still maintain relatively as high as about 24% in senescent cells. Conclusions The overexpression of p16 in senescent human fibroblasts might be related to the alteration of methylation level of exon I, its mechanisms need to be defined further.
