Increased tenascin C and DKK1 in vitiligo: possible role of fibroblasts in acral and non-acral disease
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Recently, multiple culprits—in addition to melanocytes—have been implicated in the pathogenesis of vitiligo. Among those factors are fibroblasts. However, their exact role has not been clearly elucidated. The aim of the study was to evaluate the possible role played by fibroblasts in vitiligo via studying the expression Tenascin C and DKK1 in acral versus non-acral vitiligo lesions. This case–control study included 19 non-segmental vitiligo patients and ten controls. All patients were subjected to thorough clinical evaluation. Both Tenascin C and DKK1 were measured in lesional and peri-lesional skin of acral and non-acral lesions using ELISA technique. The measured levels of Tenascin C and DKK1 were significantly higher in the vitiligo group when compared to controls in all assessed sites (P < 0.05). Tenascin C was found to be significantly higher in lesional areas compared to peri-lesional ones only in the acral sites. DKK1 was significantly higher in lesional areas in all assessed sites (P < 0.05). The current work suggests a malfunction of fibroblasts in vitiligo, through demonstrating significant up-regulation of two melanogenesis inhibitory products (Tenascin C and DKK1) in patients compared to controls. Larger scale studies are warranted to detect the possible implications of such findings on vitiligo treatment.
KeywordsVitiligo Pathogenesis Fibroblasts Tenascin C DKK1
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Conflict of interest
The authors declare that they have no conflict of interest.
There is no funding source.
This article contains studies with human participants.
Informed consent was obtained from all individual participants included in the study.
- 10.Hautmann G, Moretti S, Lotti T, Hercogova` J (2004) Pathogenesis of vitiligo: evidence for a possible ongoing disorder of the cutaneous microenvironment. In: Lotti T, Hercogova` J (eds) Vitiligo: new data and hypotheses. Marcel-Dekker, New York, pp 99–121Google Scholar