Selective down‐regulation of the α6‐integrin subunit in melanocytes by UVB light

Krengel, Sven; Stark, Imke; Geuchen, Christian; Knoppe, Bettina; Scheel, Gabriele; Schlenke, Peter; Gebert, Andreas; Wünsch, Lutz; Brinckmann, Jürgen; Tronnier, Michael

doi:10.1111/j.0906-6705.2005.00295.x

Cited by 23 publications

(26 citation statements)

References 46 publications

(42 reference statements)

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“…Laminin-1 was shown to prevent UVB-induced melanocyte apoptosis by an a6-integrin mediated mechanism. 87 These findings strengthen the impression that solar irradiation significantly influences the interplay between melanocytes, keratinocytes, and the basement membrane. These alterations might importantly contribute to the initiation and promotion of benign and malignant melanocytic neoplasms.…”

Section: Mechanisms Of Solar Nevogenesissupporting

confidence: 53%

Nevogenesis-New Thoughts Regarding a Classical Problem

Krengel¹

2005

The American Journal of Dermatopathology

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The development of melanocytic nevi is a multifactorial and heterogeneous biologic process that involves prenatal and postnatal steps. As a consequence, there are two main perspectives to nevi: that of a hamartoma and that of a benign tumor. In this review, dermatopathological studies on congenital and acquired nevi, including studies on age-related and location-dependent changes, are analyzed. These studies have lead to different hypothetical concepts on the evolution of individual lesions. In the light of findings from experimental embryology and stem cell biology, we discuss the histogenesis of nevi with special reference to the temporospatial sequence of melanocyte-basement membrane interactions and hair follicle genesis. Regarding the mechanisms of postnatal nevus development, epidemiological studies demonstrate the importance of constitutional and environmental influences, especially ultraviolet light. Possible molecular pathways of solar nevogenesis involve ultraviolet-induced alterations of the cellular microenvironment (eg, changes in the expression of cytokines and melanocyte adhesion molecules). Recent results and future directions of clinical and experimental research are presented.

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Section: Mechanisms Of Solar Nevogenesissupporting

confidence: 53%

Nevogenesis-New Thoughts Regarding a Classical Problem

Krengel¹

2005

The American Journal of Dermatopathology

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“…It does not accelerate UV carcinogenesis in mice (23). In subjects with atopic dermatitis, pimecrolimus showed minimal effect on LC (24).…”

Section: Discussionmentioning

confidence: 95%

Non-thermal atmospheric-pressure plasma can influence cell adhesion molecules on HaCaT-keratinocytes

Haertel

Wende

Woedtke

et al. 2010

Experimental Dermatology

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there was a significant difference in the number of CD83 + cells between triamcinolone-treated and pimecrolimus-treated skin (P = 0.00090) (Fig. 1, Panel 3). Discussion Triamcinolone but not pimecrolimus significantly decreased the number of CD1a + LC in the presence of UV. UV alone did not impact LC expression of CD1a. Studies support the immunosup-pressive effects of triamcinolone on LC (17), which include depletion and alteration of their morphology and function (18). In our study, UV did not decrease CD1a + LC without prior treatment with triamcinolone, and only marginally decreased CD83 expression , implying a combination effect needed for significant LC depletion. Triamcinolone treatment of irradiated skin marginally depleted HLA-DR + LC. While UV did not deplete HLA-DR expression compared with unirradiated skin, pimecrolimus caused higher HLA-DR LC expression in irradiated skin. Pimecrolimus prevented UV-induced depletion of both CD1a and CD83 expression, implying preservation of LC and their maturation. Though pimecrolimus may hinder immune barrier function of the skin (19), only limited case reports and lay articles support its carcinogenic potential (20,21). Pimecrolimus has little effect on dendritic cell maturation, in contrast to corticosteroids (9,10,22). It does not accelerate UV carcinogenesis in mice (23). In subjects with atopic dermatitis, pimecrolimus showed minimal effect on LC (24). Our study examined the effect of pimecrolimus on LC in UV-irradiated human skin for the first time. Because biopsies were performed 2 days after UV, it is possible that some of the LC had migrated from the epidermis. Additionally, LC-mediated immuno-surveillance is just one pathway against tumorigenesis. However, our results support the growing body of evidence that topical cal-cineurin inhibitors do not cause severe immunosuppression. Other experts have made similar conclusions (22,25-27). In the treatment of eczema, topical calcineurin inhibitors remain crucial as an alternative to corticosteroids. Abstract: Non-thermal atmospheric-pressure plasmas provide new hope for improvement in chronic wound management because of their potency in killing microorganisms. However, the effectiveness of the procedure has to be verified and negative effects on healthy tissues have to be excluded. In wound healing adhesion molecules play a crucial role for cell migration and proliferation. We investigated whether an atmospheric-pressure plasma jet (kINPen09) influences the expression of adhesion molecules responsible for cell-cell and cell-matrix interactions after treatment of HaCaT-keratinocytes for 10 and 30 s. Twenty-four hours after plasma treatment expression of a 2-and b 1-integrin, E-cadherin and the epidermal growth factor receptor (EGFR) was determined by flow cytometry. Plasma-treated HaCaT-cells were characterized by normal a 2-integrin and increased b 1-integrin expression. E-cadherin and EGFR expression was reduced after the 30-s treatment. We did not observe any effects following the 10-s plasma treatment. In co...

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“…It has been reported that UVB irradiation down‐regulates the expression of integrin‐α6 subunit in melanocytes but not in keratinocytes. The authors suggested that repeated sunburns may lead to the selection of a population of melanocytes which are capable of anchorage‐independent survival, culminating in solar nevogenesis and melanoma development (19). UVB irradiation also induces keratinocyte apoptosis, but it is still not clear the biological function regarding the relation between keratinocyte apoptosis and skin carcinogenesis.…”

Section: Discussionmentioning

confidence: 99%

E‐cadherin and its downstream catenins are proteolytically cleaved in human HaCaT keratinocytes exposed to UVB

Hung

Chiang

Lo³

et al. 2006

Experimental Dermatology

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It has been reported that ultraviolet B (UVB) irradiation causes the loss of E-cadherin of melanocytes, leading them to escape from neighboring keratinocytes during melanoma development. However, little has been paid on its effect on E-cadherin of keratinocytes. In the present study we therefore focus on whether UVB affects expression of E-cadherin-catenin complex in human HaCaT keratinocytes. We found that E-cadherin, beta-, and gamma-catenin but not alpha-catenin were proteolytically cleaved in UVB-irradiated HaCaT keratinocytes. The effect was only observed in keratinocyte undergoing apoptosis. Cleavage of beta- and gamma-catenin was fully abolished by caspase-3 and caspase-8 inhibitors, whereas cleavage of E-cadherin was inhibited by neither caspase nor metalloproteinase inhibitors. Functional analysis showed that the cleavage resulted in the disruption of the physical association between E-cadherin and catenins, indicating that E-cadherin signaling was compromised in UVB-irradiated HaCaT keratinocytes. Because E-cadherin in keratinocytes plays important roles in mediating cell-cell adhesion in epidermis of skin, the loss of E-cadherin and signaling components in keratinocytes may lead to the disruption of skin integrity after UVB exposure.

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Selective down‐regulation of the α6‐integrin subunit in melanocytes by UVB light

Cited by 23 publications

References 46 publications

Nevogenesis-New Thoughts Regarding a Classical Problem

Nevogenesis-New Thoughts Regarding a Classical Problem

Non-thermal atmospheric-pressure plasma can influence cell adhesion molecules on HaCaT-keratinocytes

E‐cadherin and its downstream catenins are proteolytically cleaved in human HaCaT keratinocytes exposed to UVB

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