Epigenetically altered wound healing in keloid fibroblasts.

ABSTRACT: Keloids are benign dermal tumors that form during wound healing in genetically susceptible individuals. The mechanism(s) of keloid formation is unknown and there is no satisfactory treatment. We have reported differences between fibroblasts cultured from normal scars and keloids that include a pattern of glucocorticoid resistance and altered regulation of genes in several signaling pathways associated with fibrosis, including Wnt and IGF/IGF-binding protein 5 (IGFBP5). As previously reported for glucocorticoid resistance, decreased expression of the Wnt inhibitor secreted frizzled-related protein 1 (SFRP1), matrix metalloproteinase 3 (MMP3), and dermatopontin (DPT), and increased expression of IGFBP5 and jagged 1 (JAG1) are seen only in fibroblasts cultured from the keloid nodule. In vivo,

SUBMITTER: Russell SB 

PROVIDER: S-EPMC2939920 | biostudies-literature | 2010 Oct

REPOSITORIES: biostudies-literature