Targeted killing of myofibroblasts by biosurfactant di-rhamnolipid suggests a therapy against scar formation.

ABSTRACT: Pathological myofibroblasts are often involved in skin scarring via generating contractile force and over-expressing collagen fibers, but no compound has been found to inhibit the myofibroblasts without showing severe toxicity to surrounding physiological cells. Here we report that di-rhamnolipid, a biosurfactant secreted by Pseudomonas aeruginosa, showed potent effects on scar therapy via a unique mechanism of targeted killing the myofibroblasts. In cell culture, the fibroblasts-derived myofibroblasts were more sensitive to di-rhamnolipid toxicity than fibroblasts at a concentration-dependent manner, and could be completely inhibited of their specific functions including ?-SMA expression and collagen secretion/contraction. The anti-fibrotic function of di-rhamnolipid was further verified in rabbit ear hypertrophic scar models by presenting the significant reduction of scar elevation index, type I collagen fibers and ?-SMA expression. In this regard, di-rhamnolipid treatment could be suggested as a therapy against skin scarring.

SUBMITTER: Shen C 

PROVIDER: S-EPMC5128858 | biostudies-other | 2016 Nov

REPOSITORIES: biostudies-other