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Melanosome Transfer (melanosome + transfer)

Distribution by Scientific Domains
Medical Sciences44%

Selected Abstracts

Down-Regulated PAR-2 is Associated in Part with Interrupted Melanosome Transfer in Pigmented Basal Cell Epithelioma

PIGMENT CELL & MELANOMA RESEARCH, Issue 4 2004
Kazuko Sakuraba
In pigmented basal cell epithelioma (BCE), there seems to be an abnormal transfer of melanized melanosomes from proliferating melanocytes to basaloid tumor cells. In this study, the interruption of that melanosome transfer was studied with special respect to the altered function of a phagocytic receptor, protease-activated receptor (PAR)-2 in the basaloid tumor cells. We used electron microscopy to clarify the disrupted transfer at the ultrastructural level and then performed immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) to examine the regulation of a phagocytic receptor, PAR-2, expressed on basaloid tumor cells. Electron microscopic analysis revealed that basaloid tumor cells of pigmented BCE have a significantly lower population of melanosomes (,16.4%) than do normal keratinocytes located in the perilesional normal epidermis (,91.0%). In contrast, in pigmented seborrheic keratosis (SK), a similarly pigmented epidermal tumor, the distribution of melanin granules does not differ between the lesional (,93.9%) and the perilesional normal epidermis (,92.2 %), indicating that interrupted melanosome transfer occurs in BCE but not in all pigmented epithelial tumors. RT-PCR analysis demonstrated that the expression of PAR-2 mRNA transcripts in basaloid cells is significantly decreased in pigmented BCE compared with the perilesional normal epidermis. In contrast, in pigmented SK, where melanosome transfer to basaloid tumor cells is not interrupted, the expression of PAR-2 mRNA transcripts is comparable between the basaloid tumor cells and the perilesional normal epidermis. Immunohistochemistry demonstrated that basaloid cells in pigmented BCE have less immunostaining for PAR-2 than do keratinocytes in the perilesional normal epidermis whereas in pigmented SK, there is no difference in immunostaining for PAR-2 between the basaloid tumor and the perilesional normal epidermis. These findings suggest that the decreased expression of PAR-2 in the basaloid cells is associated in part with the observed interruption of melanosome transfer in pigmented BCE. [source]

Inhibition of Melanosome Transfer from Melanocytes to Keratinocytes by Lectins and Neoglycoproteins in an In Vitro Model System

PIGMENT CELL & MELANOMA RESEARCH, Issue 3 2001
Ljiljana Minwalla
We propose that some of the critical molecules involved in the transfer of melanosomes from melanocytes to keratinocytes include plasma membrane lectins and their glycoconjugates. To investigate this mechanism, co-cultures of human melanocytes and keratinocytes derived from neonatal foreskins were established. The process of melanosome transfer was assessed by two experimental procedures. The first involved labeling melanocyte cultures with the fluorochrome CFDA. Labeled melanocytes were subsequently co-cultured with keratinocytes, and the transfer of fluorochrome assessed visually by confocal microscopy and quantitatively by flow cytometry. The second investigative approach involved co-culturing melanocytes with keratinocytes, and processing the co-cultures after 3 days for electron microscopy to quantitate the numbers of melanosomes in keratinocytes. Results from these experimental approaches indicate significant transfer of dye or melanosomes from melanocytes to keratinocytes that increased with time of co-culturing. Using these model systems, we subsequently tested a battery of lectins and neoglycoproteins for their effect in melanosome transfer. Addition of these selected molecules to co-cultures inhibited transfer of fluorochrome by approximately 15,44% as assessed by flow cytometry, and of melanosomes by 67,93% as assessed by electron microscopy. Therefore, our results suggest the roles of selected lectins and glycoproteins in melanosome transfer to keratinocytes in the skin. [source]

Effective inhibition of melanosome transfer to keratinocytes by lectins and niacinamide is reversible

EXPERIMENTAL DERMATOLOGY, Issue 7 2005
Amanda Greatens
Abstract:, Skin pigmentation results in part from the transfer of melanized melanosomes synthesized by melanocytes to neighboring keratinocytes. Plasma membrane lectins and their glycoconjugates expressed by these epidermal cells are critical molecules involved in this transfer process. In addition, the derivative of vitamin B3, niacinamide, can inhibit melanosome transfer and induce skin lightening. We investigated the effects of these molecules on the viability of melanocytes and keratinocytes and on the reversibility of melanosome-transfer inhibition induced by these agents using an in vitro melanocyte,keratinocyte coculture model system. While lectins and neoglycoproteins could induce apoptosis in a dose-dependent manner to melanocytes or keratinocytes in monoculture, similar dosages of the lectins, as opposed to neoglycoproteins, did not induce apoptosis to either cell type when treated in coculture. The dosages of lectins and niacinamide not affecting cell viability produced an inhibitory effect on melanosome transfer, when used either alone or together in cocultures of melanocytes,keratinocytes. Cocultures treated with lectins or niacinamide resumed normal melanosome transfer in 3 days after removal of the inhibitor, while cocultures treated with a combination of lectins and niacinamide demonstrated a lag in this recovery. Subsequently, we assessed the effect of niacinamide on facial hyperpigmented spots using a vehicle-controlled, split-faced design human clinical trial. Topical application of niacinamide resulted in a dose-dependent and reversible reduction in hyperpigmented lesions. These results suggest that lectins and niacinamide at concentrations that do not affect cell viability are reversible inhibitors of melanosome transfer. [source]

The discovery of the human melanocyte

PIGMENT CELL & MELANOMA RESEARCH, Issue 3 2006
Wiete Westerhof
Summary Around 2200 bc the first written description of a human pigmentation disorder, most likely vitiligo, was recorded, and from that moment the history of research into human pigmentation can be traced. For the following 4000 yr, the origins of human skin colour remained an enigma that was to generate a multitude of misconceptions. Even after European physicians began to dissect and compare dark and light coloured skin to reveal its underlying anatomy, the origins of skin and hair pigmentation were a matter of frequently erroneous speculation. The true source of human pigmentation was only finally revealed with the discovery of the melanocyte in the 19th century. Once tyrosinase was identified to be the key enzyme in pigment formation, attention focused on elucidating the chemical structure of melanin, an enterprise that remains incomplete. The developmental origins of the melanocyte were described from 1940 to 1960, and the concept of the epidermal melanin unit was introduced together with a description of the ultrastructure of the melanosome and melanosome transfer. With these advances came the realization that different skin types exhibit distinct differences at the histological level that relate to varying amounts of eumelanin and pheomelanin produced by the melanocytes. The foundation established over the past 4000 yr is the basis for all current research into this fascinating cell type. [source]

Down-Regulated PAR-2 is Associated in Part with Interrupted Melanosome Transfer in Pigmented Basal Cell Epithelioma

PIGMENT CELL & MELANOMA RESEARCH, Issue 4 2004
Kazuko Sakuraba
In pigmented basal cell epithelioma (BCE), there seems to be an abnormal transfer of melanized melanosomes from proliferating melanocytes to basaloid tumor cells. In this study, the interruption of that melanosome transfer was studied with special respect to the altered function of a phagocytic receptor, protease-activated receptor (PAR)-2 in the basaloid tumor cells. We used electron microscopy to clarify the disrupted transfer at the ultrastructural level and then performed immunohistochemistry and reverse transcription-polymerase chain reaction (RT-PCR) to examine the regulation of a phagocytic receptor, PAR-2, expressed on basaloid tumor cells. Electron microscopic analysis revealed that basaloid tumor cells of pigmented BCE have a significantly lower population of melanosomes (,16.4%) than do normal keratinocytes located in the perilesional normal epidermis (,91.0%). In contrast, in pigmented seborrheic keratosis (SK), a similarly pigmented epidermal tumor, the distribution of melanin granules does not differ between the lesional (,93.9%) and the perilesional normal epidermis (,92.2 %), indicating that interrupted melanosome transfer occurs in BCE but not in all pigmented epithelial tumors. RT-PCR analysis demonstrated that the expression of PAR-2 mRNA transcripts in basaloid cells is significantly decreased in pigmented BCE compared with the perilesional normal epidermis. In contrast, in pigmented SK, where melanosome transfer to basaloid tumor cells is not interrupted, the expression of PAR-2 mRNA transcripts is comparable between the basaloid tumor cells and the perilesional normal epidermis. Immunohistochemistry demonstrated that basaloid cells in pigmented BCE have less immunostaining for PAR-2 than do keratinocytes in the perilesional normal epidermis whereas in pigmented SK, there is no difference in immunostaining for PAR-2 between the basaloid tumor and the perilesional normal epidermis. These findings suggest that the decreased expression of PAR-2 in the basaloid cells is associated in part with the observed interruption of melanosome transfer in pigmented BCE. [source]

Inhibition of Melanosome Transfer from Melanocytes to Keratinocytes by Lectins and Neoglycoproteins in an In Vitro Model System

PIGMENT CELL & MELANOMA RESEARCH, Issue 3 2001
Ljiljana Minwalla
We propose that some of the critical molecules involved in the transfer of melanosomes from melanocytes to keratinocytes include plasma membrane lectins and their glycoconjugates. To investigate this mechanism, co-cultures of human melanocytes and keratinocytes derived from neonatal foreskins were established. The process of melanosome transfer was assessed by two experimental procedures. The first involved labeling melanocyte cultures with the fluorochrome CFDA. Labeled melanocytes were subsequently co-cultured with keratinocytes, and the transfer of fluorochrome assessed visually by confocal microscopy and quantitatively by flow cytometry. The second investigative approach involved co-culturing melanocytes with keratinocytes, and processing the co-cultures after 3 days for electron microscopy to quantitate the numbers of melanosomes in keratinocytes. Results from these experimental approaches indicate significant transfer of dye or melanosomes from melanocytes to keratinocytes that increased with time of co-culturing. Using these model systems, we subsequently tested a battery of lectins and neoglycoproteins for their effect in melanosome transfer. Addition of these selected molecules to co-cultures inhibited transfer of fluorochrome by approximately 15,44% as assessed by flow cytometry, and of melanosomes by 67,93% as assessed by electron microscopy. Therefore, our results suggest the roles of selected lectins and glycoproteins in melanosome transfer to keratinocytes in the skin. [source]

Hypermelanocytic guttate and macular segmental hypomelanosis

BRITISH JOURNAL OF DERMATOLOGY, Issue 3 2004
W. Westerhof
Summary We report two sisters, 27 and 30 years of age, with a cutaneous pigmentary anomaly, which seems to be a new entity. At the age of 26 years the elder sister developed an asymptomatic and persistent rash consisting of discrete, grouped, round to oval, guttate and nummular, hypopigmented macules, 0·2,5 cm in diameter. The distribution of the lesions was unilateral. They were located on the right side of the thorax with a moderately sharp demarcation in the mid-line and ran in a segmental distribution over the right arm, hand and fingers. Microscopic examination of lesional skin scrapings was negative for fungi. Examination with Wood's light accentuated the lesions from the surrounding normal skin. The younger sister had experienced identical, mostly guttate, skin lesions for many years, which at examination were distributed on all extremities and buttocks, and to a lesser degree on the trunk, but here in a segmental distribution. Histological examination (Masson,Fontana staining) of lesional skin of both sisters was identical. A slightly thinned epidermis and a marked decrease in pigmentation of the epidermal basal layer was seen. Electron microscopic examination of lesional skin showed an overall linear increase of morphologically and cytologically normal melanocytes just above the epidermal basal membrane. At many places the density of melanocytes was so high that the keratinocytes were displaced from the basal layer. The melanocytic dendrites extended into the suprabasal layer. The keratinocytes of lesional skin showed a decreased number of melanosomes. It is paradoxical that a hypomelanotic macule shows a histological picture of an increase in normal functioning melanocytes. In all probability a deficient melanosome transfer is responsible for this unexpected phenomenon. [source]