Endothelial-mesenchymal transition in the keloid pathogenesis

Abstract

Keloid is a fibroproliferative disorder characterized by abnormal fibrosis and increased extracellular matrix components deposition. The exact pathogenic mechanism of keloid formation is yet to be elusive, with a few known important involving factors, such as TGF-beta. Many articles have showed that fibroblasts originated from epithelial-mesenchymal transition (EMT) can be pivotal fibroblasts to form keloid tissues. More recently, several studies on the pathogenesis of fibrotic disorders are discovering the connection between endothelial mesenchymal transition (EndMT) and fibrosis. However, no article is found considering EndMT as the one of the factors in keloid pathogenesis, therefore the study on validating the involvement of EndMT in keloid tissue formation was set. Using confocal microscopy, cells in keloid tissue co-expressing platelet endothelial cell adhesion molecule-1 (PECAM-1, also known as CD31) and vimentin/ α-smooth muscle actin (α-SMA) simultaneously were recognized, and EndMT related markers were validated by checking mRNA and protein level related to the keloid formation via quantitative real-time PCR and Western blot, respectively. Only in the active keloid tissue defined by clinical activity profiles, Snail expression was increased significantly, suggesting the involvement of EndMT in keloid pathogenesis. Hence, the EndMT can be suggested to act in the keloid pathogensis as importantly as EMT.