Ultrastructure Of The Epidermal Melanocyte Dense Plate

Tarnowski, William M.

doi:10.1111/1523-1747.ep12259969

Cited by 23 publications

(15 citation statements)

References 9 publications

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“…Melanocytes presumably interact with the basement membrane through specific receptors for various matrix components, including laminin, type IV collagen, and other macromolecules. Electrondense plates associated with the basement membrane have been observed in situ in skin melanocytes (Briggaman and Wheeler, 1975;Tarnowski, 1970) and may correspond to integrin-containing focal adhesion plaques.…”

Section: Integrin Expression In Melanocytes and Melanoma Cellsmentioning

confidence: 96%

Integrin expression in malignant melanoma

Kramer

Cheng

et al. 1991

Cancer Metast Rev

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Invasion of melanoma cells into the underlying interstitial stromal matrix is the initial step for subsequent local and distant metastasis. The invading tumor cell must interact with the extracellular matrix during the early stages of invasion and later during penetration of lymphatic and blood vessels. This interaction with different types of extracellular matrix predicts that the invasive cell must possess surface adhesion receptors with diverse ligand specificities, including the capacity to bind different types of collagens and adhesive glycoproteins. Metastatic melanoma cells do in fact express multiple adhesion receptors, including several of the receptors from the integrin family of heterodimers. The integrin receptors can be either extremely specific for a single ligand or capable of binding multiple ligands. It is likely that the tumor cell's repertoire of adhesion receptors may influence not only its adhesive properties but its metastatic characteristics as well. There is evidence that normal melanocytes have an integrin profile distinct from that of melanoma cells. In particular, melanocytes adhere poorly to laminin while metastatic melanoma cells bind well to this ligand. This difference in adhesion between the two cell types appears to reflect the fact that melanoma cells express a melanoma-specific integrin (alpha 7 beta 1) that binds laminin and is not detectable in normal melanocytes. The presence of increased laminin receptors and enhanced laminin binding in melanoma cells may contribute to the malignant phenotype.

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Section: Integrin Expression In Melanocytes and Melanoma Cellsmentioning

confidence: 96%

Integrin expression in malignant melanoma

Kramer

Cheng

et al. 1991

Cancer Metast Rev

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“…The molecular interaction between melanocytes and the BM is not fully understood. Early electron microscopic investigations showed the presence of dense plates on the basal side of melanocytes, which are similar but not identical to hemidesmosomes on keratinocytes (5). By immunoelectron microscopy, Zambruno et al (6) demonstrated the presence of α3‐, α6‐, αV‐ and β1‐integrins on the melanocyte plasma membrane.…”

Section: Introductionmentioning

confidence: 99%

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

Krengel

Stark

Geuchen

et al. 2005

Experimental Dermatology

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In vivo, melanocytes bind to laminin (LM) molecules of the basement membrane (BM) via the integrins alpha3beta1 and alpha6beta1, and they adhere to neighbouring keratinocytes via E-cadherin. Only few studies have addressed the impact of ultraviolet (UV) light on the interaction of melanocytes with their microenvironment. In this report, we examined the influence of UVB irradiation on the expression of the most important melanocyte-adhesion molecules (E-, N-cadherin, alpha2-, alpha3-, alpha5-, alpha6-, alphaV-, beta1-, beta3-integrins and ICAM-1) in vitro by flow cytometry. We were able to demonstrate that the alpha6-integrin subunit is selectively and reversibly down-regulated by UVB in a dwzm 150ose-dependent manner. In comparison, keratinocytes lacked UVB-inducible alterations in the expression of alpha6-integrin. In the presence of LM-1, the UVB-induced down-regulation of alpha6-integrin in melanocytes was significantly reduced. Moreover, LM-1 increased the resistance of melanocytes to UVB-induced cell death, as measured by annexinV-binding analysis. This effect was reversed by preincubation with an alpha6-integrin-blocking antibody. By immunofluorescence, we could demonstrate that UVB leads to a dose-dependent internalization of alpha6-integrin, providing an obvious explanation for the down-regulation on the outer cell surface observed by flow cytometry. We suggest that adhesion to LM-1 through alpha6-integrin represents a protective mechanism for melanocytes to withstand UVB damage. Through alpha6-integrin internalization, sunburns might alter the interaction between melanocytes and the BM, resulting in apoptosis induced by loss of anchorage (anoikis). Repeated sunburns may then lead to the selection of a population of melanocytes which are capable of anchorage-independent survival, culminating in solar nevogenesis and melanoma development.

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“…Our data also suggest that antigen‐presenting cells are actively processing diverse, amalgamated molecules; these molecules likely include melanocytic, vascular and neural components. Significantly, the basement membrane zone of the skin contains ultrastructural irregularities 18 . The basement membrane zone underlying the melanocytes contains an electron dense plaque approximately 250–330 Å in thickness 18 .…”

Section: Discussionmentioning

confidence: 99%

“…Significantly, the basement membrane zone of the skin contains ultrastructural irregularities 18 . The basement membrane zone underlying the melanocytes contains an electron dense plaque approximately 250–330 Å in thickness 18 . Melanocytic cytoplasmic filaments do not seem to converge into this plaque.…”

Section: Discussionmentioning

confidence: 99%

“…Melanocytic cytoplasmic filaments do not seem to converge into this plaque. Instead, a 50–70 Å cytoplasmic electron dense zone abuts the internal leaflet of the trilaminar melanocyte plasma membrane and is directly apposed to adjacent keratinocytes 18 . Further, there are similarities and differences between the hemidesmosomes abutting keratinocytes and melanocytes, respectively.…”

Section: Discussionmentioning

confidence: 99%

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Autoantibodies to melanocytes and characterization of melanophages in patients affected by a new variant of endemic pemphigus foliaceus

Velez

Mihm

et al. 2011

Journal of Cutaneous Pathology

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Dermal antigen-presenting cells, including melanophages, seem to contain a diverse combination of molecules, representative of an immunologic process where these cells are engulfing both autoantigens and/or cellular debris in El Bagre-EPF. Autoantibodies to discrete components of melanocytes were also identified; the clinical and immunologic significance of these findings remains unknown. Our work may provide a possible explanation of a darkened complexion in patients affected by endemic pemphigus foliaceus.

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Ultrastructure Of The Epidermal Melanocyte Dense Plate

Cited by 23 publications

References 9 publications

Integrin expression in malignant melanoma

Integrin expression in malignant melanoma

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

Autoantibodies to melanocytes and characterization of melanophages in patients affected by a new variant of endemic pemphigus foliaceus

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