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.


METHODS
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.


CONCLUSIONS
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.
Witt
Erik
E
Plastic & Reconstructive Surgery Research, Manchester Interdisciplinary Biocentre, University of Manchester, Manchester M1 7DN, UK.
Maliri
Angeliki
A
McGrouther
Duncan Angus
DA
Bayat
Ardeshir
A