Vol.:(0123456789) 1 3 Archives of Dermatological Research https://doi.org/10.1007/s00403-018-1830-z ORIGINAL PAPER Increased tenascin C and DKK1 in vitiligo: possible role of fibroblasts in acral and non-acral disease Samia M. Esmat 1 · Heba H. El Hadidi 1 · Rehab A. Hegazy 1 · Heba I. Gawdat 1 · Amira M. Tawdy 1 · Marwa M. Fawzy 1 · Dalia M. AbdelHalim 1 · Omnia S. Sultan 1 · Olfat G. Shaker 2 Received: 3 August 2017 / Revised: 22 January 2018 / Accepted: 22 March 2018 © Springer-Verlag GmbH Germany, part of Springer Nature 2018 Abstract 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 sub- jected 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. Keywords Vitiligo · Pathogenesis · Fibroblasts · Tenascin C · DKK1 Introduction Vitiligo is a common, acquired, idiopathic disorder of the skin characterized by the onset of depigmented patches of unknown etiology and poorly understood pathogenesis [1]. Several theories have been proposed to explain its patho- genesis including genetic, autoimmune, neural, free radi- cals, biochemical, intrinsic defect, melanocytorrhagy [8], and convergent theories [2]. The ‘‘eclectic hypothesis’’ [3] emerged from the observation of the complex interactions that exist between melanocytes and other cutaneous cells such as keratinocytes, Langerhans cells, endothelial cells, fibroblasts, and mast cells [4, 5]. Fibroblasts have been put under focus, as a possible player in the complexity of vitiligo in a number of studies [6]. What adds mystery to their role is the variety of their products that have different impacts on the vitiligo course. On one hand, they secrete a set of soluble factors as hepat- ocyte growth factor, stem cell factor, and basic fibroblast growth factor, all of which are known to enhance melanocyte growth, survival, and melanogenesis [7]. Furthermore, fibro- blasts secrete matrix metalloproteinases (MMPs) and their inhibitors which are key factors in melanocyte motility and thus pigmentation [9]. On the other hand, two other products namely, Tenascin C [10] and Dickkopf1 (DKK1) [11] have been accused of having deleterious effects on pigmentation (Fig. 1). Coming in support of the fibroblasts’ negative impact on pigmentation, in 2006, Cario-Andre et al. [12] demonstrated that in vitro, human fibroblasts colonizing human dead de- epidermized dermis induced a decrease in epidermal pig- mentation. Their results proposed that fibroblast secretion might influence melanocyte proliferation and melanin dis- tribution/degradation. Furthermore, fibroblasts have been * Heba I. Gawdat [email protected] 1 Dermatology Department, Faculty of Medicine, Cairo University, 59 Street 104, Maadi Gardens, Cairo 11431, Egypt 2 Biochemistry Department, Faculty of Medicine, Cairo University, Cairo, Egypt
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