Keloid is abnormal proliferation of scar tissue beyond the original wound margins with excessive deposition of extracellular matrix (ECM) and chronic inflammation. Despite numerous previous research efforts, the pathogenesis of keloid remains unknown. There has been no functional analysis of the role of vascular endothelial cells (VECs) in the vascular morphology of keloid formation.

A new study published in Frontiers in Cell and Developmental Biology investigated gene expression patterns associated with keloid formation.

Here, living VECs were isolated from keloid tissues and gene expression patterns were investigated using microarray analysis. Five keloid tissue samples and six normal skin samples were extracted from individuals with and without keloid, respectively. Immediately after excision, living cells were isolated from tissue samples. Magnetic-activated cell sorting of VECs was performed by negative selection of fibroblasts and CD45+ cells and by positive selection of CD31+cells. After RNA extraction, gene expression analysis was carried out to compare VECs isolated from keloid tissue (KVECs) with VECs from normal skin (NVECs).

After cell isolation, the percentage of CD31+ cells as measured by flow cytometry ranged from 81.8%-98.6%. Principal component analysis was used to identify distinct molecular phenotypes in KVECs versus NVECs and these were divided into two subgroups. It was found that 15 genes were upregulated and 3 genes were downregulated in KVECs compared with NVECs. Quantitative RT-PCR and immuno his to chemistry showed 16-fold and 11-fold over expression of SERPINA3 and LAMC2, respectively.

It was stated that this the first report of VEC isolation and gene expression analysis in keloid tissue. The findings suggested that SERPINA3 and LAMC2 upregulation in KVECs may contribute to the development of fibrosis and prolonged inflammation in keloid.

Source: Frontiers in Cell and Developmental Biology. 2020 Jul 29;8:658. doi: 10.3389/fcell.2020.00658