RAC Activity in Keloid Disease: Comparative Analysis of Fibroblasts from Margin of Keloid to its Surrounding Normal Skin

Background: Keloids are characterized by excess collagen deposition within the dermis. Although the exact cause of the potentially overactive fibroblasts has yet to be elucidated, many etiological possibilities have been suggested. As fibroblasts originating from keloids appear to have an increased migration and proliferation rate, cell-signaling studies examining these factors may offer an opportunity to further our understanding of the pathogenesis of this disease. One of such cell-signaling messengers is the enzyme Ras-related C3 botulinum toxin substrate (RAC), which has never been investigated in keloid scars. Objective: This study explores the role of RAC activity in keloid disease. Method: Primary fibroblast cell lines were established from the margin of keloid (KF) scars as well as from the surrounding normal tissue (NF) from one anatomical site of the same patient. Migration and proliferation assays were performed, comparing matching NFs and KFs, and after cell lysis, RAC activity was assessed. Results: Comparing fibroblasts from 3 different patients, KFs migrated (P < .05) and proliferated (P < .05) faster than NFs. The activity levels of RAC were increased in KFs compared with NFs. Conclusion: KFs migrate and proliferate faster than NFs. RAC activity increases in KFs when compared with NFs. Inhibition of RAC could lead to a new therapeutic approach.