Melanin Transfer: A Possible Phagocytic Process*

Mottaz, Jess H.; Zelickson, Alvin S.

doi:10.1038/jid.1967.187

Cited by 103 publications

(41 citation statements)

References 6 publications

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“…The phagocytic nature of melanosome transfer has been demonstrated in vivo [10,11] and in vitro [12]. Therefore the occur rence of melanosomes within the cytoplasm of endothelial cells, pericytes and Schwann cells observed in the present study implies a DMBA-induced stimulation of melanosome phagocytosis by epithelial and nonepithelial cells.…”

Section: Discussionsupporting

confidence: 49%

Generalized Cutaneous Hyperpigmentation in Hairless Mice Induced by Topical Dimethylbenzanthracene

1989

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The skin of hairless (Ng/Bln) mice topically treated with dimethylbenzanthracene (DMBA) was investigated by light microscopy, histochemistry, electron microscopy and autoradiography in order to gain some insight into the mechanisms by which the DMBA-induced cutaneous hyperpigmentation is mediated. The results of the present study indicate that this phenomenon is due to the DMBA-induced stimulation of both the tyrosinase system and the mitotic activity of dopa-inactive dormant melanocytes.

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Section: Discussionsupporting

confidence: 49%

Generalized Cutaneous Hyperpigmentation in Hairless Mice Induced by Topical Dimethylbenzanthracene

1989

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“…In the epidermis, as well, melanocytes produce and transfer melanin to kératinocytes [22,23], Melanin-laden kératinocytes gradually degenerate and peel off. It is of great interest that the melanocytes of the inner ear always synthesize melanin, even in adult animals.…”

Section: Discussionmentioning

confidence: 99%

Development of Melanosomes and Cytochemical Observation of Tyrosinase Activity in the Inner Ear

Fukazawa

Sakagami²,

Umemoto³

et al. 1994

ORL

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The ultrastructure and tyrosinase activity of melanocytes in the inner ear of pigmented guinea pigs were observed. Melanocytes/melanocyte-like cells were seen in the stria vascularis, the vestibular dark cell area and the endolymphatic sac. In the stria vascularis, melanosomes in several stages of maturation were seen in the cytoplasm of the intermediate cells and melanin-laden endosomes existed in the basal cells. Only the intermediate cells contained tyrosinase positive cytoorganelles; Golgi sacs and neighboring small vesicles. Numerous melanocytes containing many melanosomes were observed under the epithelium of the vestibular dark cell area, and they showed tyrosinase activity. Melanocytes were seen in the endolymphatic sac, and they also showed tyrosinase activity. However, the epithelial cells of the endolymphatic sac, which had vacuoles containing melanin, did not show tyrosinase activity. Based on these findings, it can be said that (1) most of the intermediate cells of the stria vascularis must be melanocytes, (2) melanogenesis is vigorous in melanocytes of the inner ear, and (3) melanin in the epithelial cells of the endolymphatic sac is transferred in from melanocytes and is never synthesized in the epithelial cells.

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“…Normal human MCs express functional E-and P-cadherins and E-cadherin is primarily Yu responsible for adhesion of human MCs to KCs in vitro [105]. In contrast, MCs interact with KCs by transferring part of their cytoplasm with melanosome into the cytoplasm of surrounding KCs [74]. In proliferative skin, proliferating cell nuclear antigen (PCNA) expression has been observed in the nucleus of KCs and cytoplasm of MCs [52].…”

Section: Differentiation and Functional Developmentmentioning

confidence: 99%

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

2002

J Biomed Sci

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Melanocytes (MCs) are melanin-producing cells of the skin that are derived from neural crest cells. Vitiligo vulgaris is a common depigmentation disorder resulting from the destruction of functional MCs in the affected skin. The three prevailing pathomechanisms of vitiligo are the immune hypothesis, the neural hypothesis and the autocytotoxic hypothesis. None of these mechanisms has been conclusively proven. Melanoblasts (MBs) in the outer root sheath of the hair follicles are the reservoir cells for repigmentation. Recovery from vitiligo is initiated by activation and proliferation of these MBs, followed by upward migration to the nearby epidermis that forms perifollicular pigmentation islands. Migration, proliferation and differentiation of MCs and MBs are regulated by keratinocyte-derived factors and some coat color genes. Any therapy for vitiligo must explain not only the repopulation of MCs but also their functional development. In patients with vitiligo, MCs are destroyed in the skin, the eyes, and possibly the ears. However, the concept of vitiligo as a systemic disease will be clearly established only when the mechanisms involved in vitiligo are identified. Recent advances in the fields of neural crest cell culture and molecular genetics have opened new perspectives in the understanding of vitiligo. Not only will this result in better treatments for vitiligo patients, but possibly will also provide a key to triggering nerve cell regrowth in other nervous diseases.

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Melanin Transfer: A Possible Phagocytic Process*

Cited by 103 publications

References 6 publications

Generalized Cutaneous Hyperpigmentation in Hairless Mice Induced by Topical Dimethylbenzanthracene

Generalized Cutaneous Hyperpigmentation in Hairless Mice Induced by Topical Dimethylbenzanthracene

Development of Melanosomes and Cytochemical Observation of Tyrosinase Activity in the Inner Ear

Melanocyte Destruction and Repigmentation in Vitiligo: A Model for Nerve Cell Damage and Regrowth

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