The methylation pattern of p16^INK4agene promoter in psoriatic epidermis and its clinical significance

Abstract

Overall, methylation of the p16INK4a gene promoter is found in psoriatic epidermis, which is associated with the mRNA level of p16INK4a expression and activity of the disease. These data indicate that methylation of the p16INK4a promoter may play a potential role in the pathogenesis of psoriasis.

The Genetics of Human Skin Disease

“…Similarly, hypomethylation of p16INK4A (antiapoptotic gene) has been reported in psoriasis, along with demethylation of one of the promoters of the SHP-1 gene, important for keratinocyte growth and proliferation (Ruchusatsawat et al 2006;Zhang et al 2007;Chen et al 2008). Importantly, the findings from these studies provides additional evidence that the molecular defects underlying polygenic skin diseases transcend single-gene mutations, and may be characterized by more global changes at the chromatin level associated with a multitude of downstream effects on gene expression.…”

An immunohistochemical study of the distribution of p 16 protein in oral mucosa in smokers, non-smokers and in frictional keratosis

“…The present results demonstrated that normal oral epithelium in non-smokers does not express p16 at the immunohistochemical level. Chen et al (14) have indicated that methylation of the p16INK4a promoter may play a potential role in the pathogenesis of psoriasis. Nuclear p16 protein is detectable by immunohistochemistry, at the threshold of sensitivity used in this study, in a proportion of fibroblasts and endothelial cells in the lamina propria.…”

Genome-Wide DNA Methylation Profiling in Diabetogenic and Regulatory T Cells from NOD Mice

“…Based on these genome-wide analyses, our studies have found that Tpaths and Tregs have different methylation density distribution in their autosomes and chromosome X. These novel results suggest epigenetic differences may contribute to the functional differentiation/specification of Tpaths vs. Tregs [29][30][31][32][33][34][35][36][37][38][39][40][41][42][43].…”

“…[37], and p16, SHP1, p15, and p21 in psoriasis [38][39][40]. The overexpression of two methyl CpG -binding domain (MBD) proteins, MBD2 and MBD4, may assoiated with the DNA hypomethylation in SLE CD4 + T cells [41].…”