Identification of Differentially Methylated CpG Sites in Fibroblasts from Keloid Scars.

摘要: As a part of an abnormal healing process dermal injuries and irritation, keloid scars arise on the skin as benign fibroproliferative tumors. Although etiology scarring remains unsettled, considerable recent evidence suggested that keloidogenesis may be driven by epigenetic changes, particularly, DNA methylation. Therefore, genome-wide scanning methylated cytosine-phosphoguanine (CpG) sites in extracted from 12 scar fibroblasts (KF) control (CF) (six normal six normotrophic fibroblasts) was conducted using Illumina Human Methylation 450K BeadChip two replicates for each sample. Comparing KF CF used Linear Models Microarray Data (Limma) model revealed 100,000 differentially (DM) CpG sites, 20,695 which were found to hypomethylated 79,305 hypermethylated. The top DM associated with TNKS2, FAM45B, LOC723972, GAS7, RHBDD2 CAMKK1. Subsequently, most functionally enriched genes 100 significantly (p ≤ 0.05) SH2 domain binding, regulation transcription, DNA-templated, nucleus, positive protein targeting mitochondrion, nucleoplasm, Swr1 complex, histone exchange, cellular response organic substance. In addition, NLK, CAMKK1, LPAR2, CASP1, NHS showed common regulators signaling network analysis. Taken together, these findings shed light methylation status keloids could implicated underlying mechanism formation remission.