Tissue expression of aquaporin 3 in different sites of vitiligo: an immunohistochemical study

Esmat, Samia; Zeid, Ola Abu; Halim, Dalia M. Abdel; Fawzy, M.T.; Latif, Mahmoud Abdel; Lazarova, V.; Assaf, Magda

doi:10.1111/jdv.15049

Cited by 7 publications

(9 citation statements)

References 11 publications

(3 reference statements)

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“…Best cut‐off value for HBD‐1 in vitiligo patients before NBUVB is 58.9 with 96% sensitivity and 100% specificity, and after NBUVB is 90.5 with 100% sensitivity and 64% specificity; indicating the overall accuracy of HBD‐1 to predict cases as shown in Figure1 and Table 1. This study results signify that low HBD‐1 levels in lesional vitiligo skin could be one of the results of impaired keratinocytes function as well as defective epidermal barrier in vitiligo which was previously affirmed in a number of studies 3,6,7 . Also, these results are in concordance with Ochoa‐Ramírez et al, 4 who found similar results to ours, albeit they conducted their study on serum of 80 vitiligo patients and their matched healthy controls.…”

Section: Resultssupporting

confidence: 91%

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Estimation of tissue level of human beta‐defensin 1 in vitiligo before and after narrowband ultraviolet B phototherapy: A case‐control study

Zaher

Shawky²,

Rashed

et al. 2021

Photoderm Photoimm Photomed

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Defensins, a class of cationic arginine-rich antimicrobial peptides (AMPs), are small peptides with three known subfamilies: α-, β-, and θ-defensins. 1 Beta-defensins have an essential role in the innate immunity toward microbes, and in particular, at the epithelial interface. 2 The etiopathogenesis of vitiligo is believed to be complex. There is an evidence that epidermal keratinocytes has an imminent role in the pathogenesis of vitiligo based upon the fact that both keratinocytes and melanocytes form a single structural and functional unit. 3 Genotype frequencies of HBD-1 were studied in vitiligo patients.Both the -44CG genotype and G-allele frequencies were higher in patients with vitiligo, conferring an increased risk of developing vitiligo. 4,5 Therefore, the goal of this study was to assess the tissue level of HBD-1 in vitiligo patients in comparison to its level in healthy controls to verify its role in the pathogenesis of vitiligo. | SUBJEC TS AND ME THODSRecruitment of cases took place at the Dermatology outpatient clinic, Kasr AlAiny, Faculty of Medicine, Cairo University. The study was conducted on 34 patients with non-segmental vitiligo; 25 continued while nine patients dropped out as well as 25 healthy controls (who were not subjected to any treatment) over a period of 12 months from March/2019 to March/2020. The recruited patients

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Section: Resultssupporting

confidence: 91%

“…The etiopathogenesis of vitiligo is believed to be complex. There is an evidence that epidermal keratinocytes has an imminent role in the pathogenesis of vitiligo based upon the fact that both keratinocytes and melanocytes form a single structural and functional unit 3 …”

Section: Introductionmentioning

confidence: 99%

Estimation of tissue level of human beta‐defensin 1 in vitiligo before and after narrowband ultraviolet B phototherapy: A case‐control study

Zaher

Shawky²,

Rashed

et al. 2021

Photoderm Photoimm Photomed

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“…Downregulation of AQP3 leads to significantly reduced expression of E‐cadherin and catenins resulting in decreased keratinocyte adhesion and survival and increased apoptosis in cultured normal human keratinocytes and in vitiligo 15–17 …”

Section: Discussionmentioning

confidence: 99%

“…Downregulation of AQP3 leads to significantly reduced expression of E-cadherin and catenins resulting in decreased keratinocyte adhesion and survival and increased apoptosis in cultured normal human keratinocytes and in vitiligo. [15][16][17] The interplay between E-cadherin and β-catenin, which is crucial for the homeostasis of cell adhesion, is regulated by phosphorylation sites, the mutation of which weakens cell adhesiveness. [18][19][20] AQP3 is involved indirectly in several phosphorylation pathways through its glycerol transport function.…”

Section: Discussionmentioning

confidence: 99%

Downregulation of aquaporin 3 in patients with pemphigus vulgaris

Mahmoud

Saleh

Aziz

et al. 2022

Wound Repair Regeneration

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Pemphigus vulgaris (PV) is an autoimmune bullous skin disease. Aquaporin 3 (AQP3) is a glycerol/water channel involved in several physiological functions. Evaluation of the tissue expression and localization of AQP3 in the skin of PV patients. Twentyseven PV patients and 30 controls were included. The patients were subjected to history taking, clinical evaluation, Autoimmune Bullous Skin Disorder Intensity Score and 4-mm punch biopsy. The biopsies were stained using anti-human AQP3 antibody and the immunofluorescence pattern and intensity were evaluated using a scoring system and ImageJ software analysis. AQP3 was expressed in the basal epidermis in 27 (100%) and in the suprabasal epidermis in 19 PV patients (70.4%). It was expressed in all controls in basal and suprabasal layers. Intensity of AQP3 immunofluorescence was strong in 2 (7.4%), moderate in 19 (70.4%) and weak in 6 patients (22.2%) while it was strong in 18 (60%) and moderate in 12 controls (40%). AQP3 expression was significantly lower in patients than controls in the suprabasal epidermis (p = 0.001). Patients with extensive disease had significantly weaker AQP3 intensity than those with marked disease (p = 0.005) Downregulation of AQP3 in patients with PV, especially in the suprabasal layers and in extensive clinical disease, suggests a potential role of AQP3 in the pathogenesis of PV.

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“…In skin reconstruct model, fibroblasts induced a decrease in pigmentation when compared with reconstruct model without fibroblasts. [ 3–66 ] However, at present, none of the studies concerning the dermis has documented alterations in the amount of fibroblasts underlying vitiligo lesion. In addition to paracrine contribution to skin integrity, dermal fibroblasts also drive the structural framework for tissue, determining thickness and firmness of skin by the synthesis and deposition of extracellular matrix and basement membrane proteins, such as collagen I, collagen IV, fibronectin, fibrillin, elastin and tenascin.…”

Section: Introductionmentioning

confidence: 99%

Involvement of non‐melanocytic skin cells in vitiligo

Bastonini

Bellei

Filoni

et al. 2019

Experimental Dermatology

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Despite melanocytes are the key players in vitiligo, a continuous cross‐talk between epidermal and dermal cells may strictly affect their functionality, in both lesional skin and non‐lesional skin. Focusing on this interplay, we have reviewed existing literature supporting evidence on cellular and functional alterations of surrounding epidermal keratinocytes, extracellular matrix (ECM) proteins and fibroblasts in the underlying dermal compartment that may contribute to melanocyte disappearance in vitiligo. We have also examined some clinical and therapeutic aspects of the disease to sustain the non‐exclusive involvement of melanocytes within vitiligo. As a result, a different and more complex scenario has appeared that may enable to provide better understanding about origins and progress of vitiligo and that should be considered in the evaluation of new treatment approaches.

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Tissue expression of aquaporin 3 in different sites of vitiligo: an immunohistochemical study

Cited by 7 publications

References 11 publications

Estimation of tissue level of human beta‐defensin 1 in vitiligo before and after narrowband ultraviolet B phototherapy: A case‐control study

Estimation of tissue level of human beta‐defensin 1 in vitiligo before and after narrowband ultraviolet B phototherapy: A case‐control study

Downregulation of aquaporin 3 in patients with pemphigus vulgaris

Involvement of non‐melanocytic skin cells in vitiligo

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