Transcriptional profiling of rapamycin-treated fibroblasts from hypertrophic and keloid scars
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Updated: Apr 29, 2026
In Vitro Model of Human Cutaneous Hypertrophic Scarring using Macromolecular Crowding
Published on: May 1, 2020
Victor W Wong1, Fanglei You, Michael Januszyk
1From the *Division of Plastic and Reconstructive Surgery, Department of Surgery, Oregon Health and Science University, Portland, OR; and †Division of Plastic and Reconstructive Surgery, Department of Surgery, Stanford University, Stanford, CA.
Abstract:
Excess scar formation after cutaneous injury can result in hypertrophic scar (HTS) or keloid formation. Modern strategies to treat pathologic scarring represent nontargeted approaches that produce suboptimal results. Mammalian target of rapamycin (mTOR), a central mediator of inflammation, has been proposed as a novel target to block fibroproliferation. To examine its mechanism of action, we performed genomewide microarray on human fibroblasts (from normal skin, HTS, and keloid scars) treated with the mTOR inhibitor, rapamycin. Hypertrophic scar and keloid fibroblasts demonstrated overexpression of collagen I and III that was effectively abrogated with rapamycin. Blockade of mTOR specifically impaired fibroblast expression of the collagen biosynthesis genes PLOD, PCOLCE, and P4HA, targets significantly overexpressed in HTS and keloid scars. These data suggest that pathologic scarring can be abrogated via modulation of mTOR pathways in procollagen and collagen processing.
