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Cultured Melanocytes (cultured + melanocyte)
Selected AbstractsAutologous Cultured Melanocytes in Vitiligo TreatmentDERMATOLOGIC SURGERY, Issue 9 2007RAFAL CZAJKOWSKI MD BACKGROUND Surgical treatment of vitiligo is indicated when lesions are localized in poorly responding areas. OBJECTIVES The objectives were: (1) to establish the melanocyte culture obtained from the epidermis of vitiligo patients for future treatment; (2) to estimate the influence of selected factors on the formation of suction blisters and the results of culture; and (3) to compare the results of treatment of vitiliginous macules localized in the dorsum of the hands and lower limbs by transplantation of cultured autologous melanocytes plus psoralen and ultraviolet A (PUVA) therapy (CMP), suction blister transplantation plus PUVA therapy (SBP), cryotherapy plus PUVA-therapy (CP), and only PUVA therapy (OP). METHODS Forty patients were qualified for the study. The roofs of the suction blisters were used as a melanocyte source for culture establishment or were directly transplanted. RESULTS The CMP procedure was successfully performed on only 10 of 20 patients because of the difficulties in cell culture establishment. The SBP method was carried out on all 20 patients. A total lack of effectiveness was found in CP and OP methods. CONCLUSIONS The effectiveness of culture depends on time of suction blister forming, phototype, and previous PUVA therapy. This study demonstrated the advantage of the SBP over the CMP method. [source] Melanin Offers Protection Against Induction of Cyclobutane Pyrimidine Dimers and 6,4 Photoproducts by UVB in Cultured Human Melanocytes,PHOTOCHEMISTRY & PHOTOBIOLOGY, Issue 3 2001Nico P. M. Smit ABSTRACT The goal of this investigation was to correlate the melanin content in human pigmentary cells with the generation of UVB-induced photoproducts and to examine the relationship between the melanin content and the removal of the photoproducts. Cultured melanocytes from light-skinned individuals synthesized less melanin and produced more cyclobutane pyrimidine dimers and 6,4 photoproducts upon UVB exposure than did melanocytes from black skin. Tyrosine-stimulated melanogenesis provided protection against DNA damage in both cell types. In another set of pigmented cell lines a ratio between eumelanin and pheomelanin was determined. The assessment of association between DNA damage induction and the quantity and quality of melanin revealed that eumelanin concentration correlated better with DNA protection than pheomelanin. Skin type,I and skin type,VI melanocytes, congenital nevus (CN)-derived cells and skin type,II melanocytes from a multiple-melanoma patient were grown in media with low or high l -tyrosine concentration. The cells were irradiated with 200 J/m2 UVB, and the levels of the photoproducts were determined immediately and after 6 and 24 h. Once again the induction of the photoproducts was mitigated by increased melanogenesis, and it was inversely correlated with the skin type. No significant differences were found for the removal of photoproducts in the cultures of skin types I and VI and CN cells. No indications of a delay in the removal of photoproducts in the melanocytes from the multiple-melanoma patient were found either. [source] Low-energy helium,neon laser induces melanocyte proliferation via interaction with type IV collagen: visible light as a therapeutic option for vitiligoBRITISH JOURNAL OF DERMATOLOGY, Issue 2 2009C-C.E. Lan Summary Background, The treatment of vitiligo remains a challenge for clinical dermatologists. We have previously shown that the helium,neon laser (He,Ne laser, 632·8 nm) is a therapeutic option for treatment of this depigmentary disorder. Objectives, Addressing the intricate interactions between melanocytes, the most important cellular component in the repigmentation scheme of vitiligo, and their innate extracellular matrix collagen type IV, the current study aimed to elucidate the effects of the He,Ne laser on melanocytes. Methods, Cultured melanocytes were irradiated with the He,Ne laser. Relevant biological parameters including cell attachment, locomotion and growth were evaluated. In addition, the potentially involved molecular pathways were also determined. Results, Our results show that in addition to suppressing mobility but increasing attachment to type IV collagen, the He,Ne laser stimulates melanocyte proliferation through enhanced ,2,1 integrin expression. The expression of phosphorylated cyclic-AMP response element binding protein (CREB), an important regulator of melanocyte growth, was also upregulated by He,Ne laser treatment. Using a specific mitochondrial uncoupling agent [carbonyl cyanide m-chlorophenyl-hydrazone (CCCP)], the proliferative effect of the He,Ne laser on melanocytes was abolished and suppression of melanocyte growth was noted. Conclusions, In summary, we have demonstrated that the He,Ne laser imparts a growth stimulatory effect on functional melanocytes via mitochondria-related pathways and proposed that other minor pathways including DNA damage may also be inflicted by laser treatment on irradiated cells. More importantly, we have completed the repigmentation scheme of vitiligo brought about by He,Ne laser light in vitro and provided a solid theoretical basis regarding how the He,Ne laser induces recovery of vitiligo in vivo. [source] Vitamin D and systemic cancer: is this relevant to malignant melanoma?BRITISH JOURNAL OF DERMATOLOGY, Issue 2 2002J.E. Osborne Summary 1,25-dihydroxyvitamin D3[1,25(OH)2D3] is a well-known potent regulator of cell growth and differentiation and there is recent evidence of an effect on cell death, tumour invasion and angiogenesis, which makes it a candidate agent for cancer regulation. The classical synthetic pathway of 1,25(OH)2D3 involves 25- and 1,-hydroxylation of vitamin D3, in the liver and kidney, respectively, of absorbed or skin-synthesized vitamin D3. There is recent focus on the importance in growth control of local metabolism of 1,25(OH)2D3, which is a function of local tissue synthetic hydroxylases and particularly the principal catabolizing enzyme, 24-hydroxylase. The classical signalling pathway of 1,25(OH)2D3 employs the vitamin D nuclear receptor (VDR), which is a transcription factor for 1,25(OH)2D3 target genes. Effects of this pathway include inhibition of cellular growth and invasion. Cytoplasmic signalling pathways are increasingly being recognized, which similarly may regulate growth and differentiation but also apoptosis. 1,25(OH)2D3 has a major inhibitory effect on the G1/S checkpoint of the cell cycle by upregulating the cyclin dependent kinase inhibitors p27 and p21, and by inhibiting cyclin D1. Indirect mechanisms include upregulation of transforming growth factor-, and downregulation of the epidermal growth factor receptor. 1,25(OH)2D3 may induce apoptosis either indirectly through effects on the insulin-like growth receptor and tumour necrosis factor-, or more directly via the Bcl-2 family system, the ceramide pathway, the death receptors (e.g. Fas) and the stress-activated protein kinase pathways (Jun N terminal kinase and p38). Inhibition of tumour invasion and metastasis potential has been demonstrated and mechanisms include inhibition of serine proteinases, metalloproteinases and angiogenesis. The lines of evidence for an effect of vitamin D3 in systemic cancer are the laboratory demonstration of relevant effects on cellular growth, differentiation, apoptosis, malignant cell invasion and metastasis; epidemiological findings of an association of the occurrence and outcome of cancers with derangements of vitamin D3/1,25(OH)2D3 and the association of functional polymorphisms of the VDR with the occurrence of certain cancers. In addition, vitamin D3 analogues are being developed as cancer chemotherapy agents. There is accumulating evidence that the vitamin D3/1,25(OH)2D3/VDR axis is similarly important in malignant melanoma (MM). MM cells express the VDR, and the antiproliferative and prodifferentiation effects of 1,25(OH)2D3 have been shown in cultured melanocytes, MM cells and MM xenografts. Recently, an inhibitory effect on the spread of MM cells has been demonstrated, low serum levels of 1,25(OH)2D3 have been reported in MM patients and the VDR polymorphisms have been shown to be associated with both the occurrence and outcome of MM. The relationship between solar irradiation and MM is more complex than for the systemic cancers. As in other cancers, there is evidence of a protective effect of vitamin D3 in MM, but ultraviolet radiation, which is a principal source of vitamin D3, is mutagenic. Further work is necessary on the influence of serum vitamin D3 levels on the occurrence and prognosis of MM, the effects of sun protection measures on serum vitamin D3 levels in temperate climates and epidemiological studies on geographical factors and skin type on the prognosis of MM. Meanwhile, it would seem mandatory to ensure an adequate vitamin D3 status if sun exposure were seriously curtailed, certainly in relation to carcinoma of breast, prostate and colon and probably also MM. [source] | ||||||||||