Potential treatment of keloid pathogenesis with follistatin 288 by blocking the activin molecular pathway

a.sfakia shared this article with you from Inoreader Potential treatment of keloid pathogenesis with follistatin 288 by blocking the activin molecular pathway Via Experimental Dermatology Abstract Keloids are benign tumours caused by abnormal wound healing driven by increased expression of cytokines, including activin A. This study compared effects of activins on normal and keloid‐derived human dermal fibroblasts and investigated a novel treatment for keloids using follistatin. Normal skin and keloid tissue samples from 11 patients were used to develop primary fibroblast cultures, which were compared in terms of their histology and relevant gene (qRT‐PCR and RNAseq) and protein (ELISA) expression. Activin A (INHBA) and connective tissue growth factor (CTGF) gene expression were significantly upregulated in keloid fibroblasts, as was activin A protein expression in cell lysates and culture medium. Activator protein 1 inhibitor (SR11302) significantly decreased INHBA and CTGF expression in keloid fibroblasts and a single treatment of follistatin over five days significantly inhibited activin and various matrix‐related genes in keloid fibrobla sts when compared to controls. Follistatin, by binding activin A, suppressed CTGF expression suggesting a novel therapeutic role in managing keloids and perhaps other fibrotic diseases. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.