Abstract
Keloids, benign cutaneous overgrowths of dermal fibroblasts, are caused by pathologic scarring of wounds during healing. Current surgical and therapeutic modalities are unsatisfactory. Although adiponectin has shown an antifibrotic effect, its large size and insolubility limit its potential use in keloid treatment. We investigated the effect of a smaller and more stable adiponectin-based peptide (ADP355) on transforming growth factor β1 (TGF-β1)-induced fibrosis in a primary culture of keloid fibroblasts prepared from clinically obtained keloid samples. Xenograft of keloid tissues on athymic nude mice was used to investigate the effect of intralesional injection of ADP355. ADP355 significantly attenuated the TGF-β1-induced expression of procollagen type 1 in keloid fibroblasts (p < 0.05). Moreover, it inhibited the TGF-β1-induced phosphorylation of SMAD3 and ERK, while amplifying the phosphorylation of AMP-activated protein kinase (p < 0.05). Knockdown of adiponectin receptor 1 reversed the attenuation of procollagen expression in ADP355-treated TGF-β1-induced fibrosis (p < 0.05). ADP355 also significantly reduced the gross weight and procollagen expression of keloid tissues in xenograft mice compared to control animals. These results demonstrate the therapeutic potential of the adiponectin peptide ADP355 for keloids.
Highlights
Keloids are a type of excessive scarring, which results from aberrations in physiologic wound healing
We investigated the effect of ADP355 in keloid fibroblasts
Keloid formation is the consequence of the pathologic wound healing process, which involves
Summary
Keloids are a type of excessive scarring, which results from aberrations in physiologic wound healing They generally occur after apparent injury to the skin tissue but may develop over several years after minor injuries and may even form spontaneously without any perceivable injuries. Keloids persist for long periods and do not regress spontaneously [1] This condition is characterized by benign cutaneous hyperproliferation of dermal fibroblasts; overproduction of collagen, fibronectin and other extracellular matrix components; and increased infiltration of inflammatory cells with high recurrence rates [2,3]. These lesions can significantly affect the patient’s quality of life, both physically and psychologically. Current therapeutic modalities often exhibit limited efficacies [4]
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