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 α-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 α-SMA expression. In this regard, di-rhamnolipid treatment could be suggested as a therapy against skin scarring.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Actins / antagonists & inhibitors
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Actins / genetics
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Actins / metabolism
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Animals
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Cell Differentiation
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Cicatrix, Hypertrophic / drug therapy*
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Cicatrix, Hypertrophic / genetics
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Cicatrix, Hypertrophic / metabolism
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Cicatrix, Hypertrophic / pathology
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Collagen Type I / antagonists & inhibitors
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Collagen Type I / genetics
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Collagen Type I / metabolism
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Ear / injuries
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Fibroblasts / drug effects*
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Fibroblasts / metabolism
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Fibroblasts / pathology
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Gene Expression
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Glycolipids / isolation & purification
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Glycolipids / pharmacology*
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Male
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Molecular Targeted Therapy
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Myofibroblasts / drug effects*
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Myofibroblasts / metabolism
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Myofibroblasts / pathology
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Pseudomonas aeruginosa / chemistry
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Pseudomonas aeruginosa / physiology
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Rabbits
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Skin / drug effects
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Skin / injuries
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Surface-Active Agents / isolation & purification
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Surface-Active Agents / pharmacology*
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Surgical Wound / drug therapy*
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Surgical Wound / genetics
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Surgical Wound / metabolism
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Surgical Wound / pathology
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Wound Healing / drug effects
Substances
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Actins
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Collagen Type I
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Glycolipids
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Surface-Active Agents
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rhamnolipid hemolysin, Pseudomonas aeruginosa