Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P20020 (adenosine triphosphatase)
 3,299 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Dispersed cell cultures of guinea-pig epidermis have been maintained for up to 36 days. The progress of these cultures has been studied by phase contrast microscopy, the adenosine triphosphatase reaction, and cinephotomicrography. Langerhans cells have been identified and their behaviour studied, particularly in relation to keratinocytes.
Br J Dermatol 1975 Feb
PMID:Langerhans cells in tissue cultures of guinea-pig epidermal cells. 12 92

We describe a mother and two daughters who had the following clinical manifestations: bluish discoloration of the vermillion ridge of the lips, nipple areolae, and nail beds; discrete telangiectasia of the chest, elbows, and dorsa of the hands; varicosities of the lower part of the legs; and (in the two daughters) migraine headaches. Routine histologic examination of tissue from the lips and elbows disclosed extensive, dilated, horizontal subpapillary telangiectases. Enzyme histochemical stains demonstrated activity of adenosine triphosphatase and leucine aminopeptidase around these dilated vessels. Alkaline phosphatase activity was strikingly absent from the dilated subpapillary vessels. By electron microscopy, these vessels were demonstrated to be postcapillary venules. We propose an autosomal dominant mode of inheritance.
Arch Dermatol 1979 Apr
PMID:Hereditary acrolabial telangiectasia. A report of familial blue lips, nails, and nipples. 43 75

In the guinea pig, the epidermal Langerhans cells studied by adenosine triphosphatase and electron microscopic techniques in dinitrochlorobenzene-induced contact dermatitis showed early cellular vacuolar and granular changes and intraepidermal contact with mononuclear cells. At later periods of up to 48 hours, the Langerhans cells migrated to the surface of a thickened epidermis and were lost in the parakeratotic horny layer that was shed. Thus, the Langerhans cell probably has a macrophage-type role in the epidermal reaction of contact dermatitis, and as the sponglosis and the inflammatory reaction develop, these cells are shed with the degenerating keratinocytes.
Arch Dermatol 1978 Sep
PMID:Langerhans cells in contact dermatitis of the guinea pig. 68 44

The C57Bl/Ler-vit.vit mouse grows a black pelage after birth. During successive hair molts, the fur loses its pigmentation. By 6 months of age, most of the fur of the animal is white. The epidermis of the ears and tail also loses its pigmentation. Histologic studies confirm that in the epidermis and hair follicles there is an absence of pigment cells identifiable by various histochemical or electron microscopic techniques. This mouse may be an excellent model in which to study the role of Langerhans' cells and the immune response in the pathogenesis of vitiligo, a study not easily done in humans. From results of prior studies, we postulated that if Langerhans' cells were involved in the destruction of melanocytes, they would be abnormal (either more or less numerous) in number during the active phase of depigmentation and normal in number after depigmentation was complete. To determine whether the Langerhans cell (Ia+/adenosine triphosphatase dendritic epidermal cell) might be involved in destruction of pigment cells, we quantified the number of Ia+ and adenosine triphosphatase dendritic cells in the hair follicles in skin from the ear, abdomen, back, and tail from male C57Bl/Ler-vit.vit mice while the fur and skin were depigmenting and after depigmentation was almost completed. We found that Langerhans' cells were normal in number during depigmentation and were most numerous after depigmentation. Previous studies indicate that Langerhans' cells in these mice are functionally defective and respond poorly to some contact allergens. From these morphologic and functional data, we conclude that Langerhans' cells probably are uninvolved in causing depigmentation in these mice. We also observed that the epithelium of hair follicles has a significantly higher (up to 1600/mm2) population density of Langerhans' cells than interfollicular skin.
Arch Dermatol 1987 Aug
PMID:Langerhans' cells in hair follicles of the depigmenting C57Bl/Ler-vit.vit mouse. A model for human vitiligo. 244 80

The exposure of murine skin to potent chemical carcinogens induced distinctive effects on the distribution of epidermal Langerhans cells (LC). Our previous finding that weekly applications of 7,12-dimethylbenz[a]anthracene deplete the numbers of adenosine triphosphatase (ATPase)-positive LC was extended to show that LC are also depleted on Ia and beta-glucuronidase staining. In contrast, application of the tobacco-derived carcinogen, benzo[a]pyrene (BP), caused a significant increase in Ia-positive LC density within 2 weeks and elevated levels were maintained for up to 6 months with continuous treatment. The tobacco-derived cocarcinogenic agent, catechol, also enhanced the numbers of epidermal LC. The LC in carcinogen treated epidermis were morphologically abnormal; after BP and catechol treatment LC appeared smaller with shorter dendrites, whereas in DMBA treated epidermis LC were enlarged with elongated dendrites. Application of the contact sensitizing agent, dinitrofluorobenzene, to skin treated with BP induced hyporesponsiveness rather than contact sensitivity upon subsequent antigen challenge. Hence, the function of the large number of morphologically altered LC in BP treated skin was impaired. We conclude that carcinogen-induced alterations of LC are associated with impaired immunocompetence, although different carcinogens probably operate via different mechanisms to induce such phenomena.
J Invest Dermatol 1989 Feb
PMID:Differential effects of benzo[a]pyrene and dimethylbenz[a]-anthracene on Langerhans cell distribution and contact sensitization in murine epidermis. 249 54

Epidermal Langerhans cells (LCs) are bone marrow-derived immune cells in the epidermis. Recently, we reported that adenosine triphosphatase (ATPase)-positive LC density in the hind-limb skin of male mice was lower than that of female and that orchiectomy resulted in an increase in LC density, though ovariectomy had no significant effect. To further investigate the control mechanisms of sex differences in LC density, the effect of systemic and topical application of testosterone propionate (TP) on LC density was examined in C57BL/6 mice. Subcutaneous injections of TP 5.8 X 10(-8) mol (20 micrograms)/day/mouse for 14 d resulted in a significant decrease in LC density both in orchiectomized males and normal females, and such an effect was also observed in adrenalectomized mice, suggesting that this effect of TP is not indirectly mediated by glucocorticosteroids. TP was also effective when applied as an ointment (1% or 5%) to the right hind-limb skin of both orchiectomized males and normal females for 14 d; namely, the LC density of the right hind-limb was lower than that of the left. Beta-estradiol and progesterone 5.8 X 10(-8) mol/day/mouse had no significant effect on LC density when systemically applied for 14 d to normal males and females. These results suggest that sex differences in LC density may result from higher concentrations of testosterone or its metabolites in males, and that the function of testosterone may be local.
J Invest Dermatol 1989 Jan
PMID:Effect of systemic and topical application of testosterone propionate on the density of epidermal Langerhans cells in the mouse. 264 15

This study reviews data on the histogenesis of Kaposi's sarcoma and angiosarcoma derived from clinical features, histology, electron microscopy, enzyme histochemistry, and immunochemistry of both diseases. Their hemorrhagic clinical appearance contrasts the predominantly lymphatic histologic features of vessels in early lesions. Investigations performed to resolve the debate whether these tumors arise from blood vessel or lymphatic endothelium show remarkably similar results for both conditions. Electron microscopy reveals Weibel - Palade bodies in a minority of cases, but features consistent with less well-differentiated blood vessel endothelium may be seen in a greater proportion of tumors. Enzyme histochemistry generally shows absence of adenosine triphosphatase and alkaline phosphatase in tumor cells; a pattern of enzymes similar to that found in normal lymphatic endothelium. Conflicting data arises from the large number of immunohistochemical studies performed on both conditions. Factor VIII-related antigen and Ulex europaeus agglutinin-I have been most frequently employed, but the specificity of these agents for blood vessel endothelium is debatable. Panendothelial markers show consistent labeling of both tumors, but marker studies employing a wide range of monoclonal antibodies specific for blood vessel endothelium have shown occasional positive labeling of tumor cells. A number of studies have claimed absence of labeling with specific blood vessel monoclonal antibodies, but at present no study employing a specific marker for lymphatic endothelium has been reported. Although the demonstration of specific markers for blood vessel endothelium in these tumors has been variable, the data would be compatible with lesions arising from undifferentiated stem cells that proliferate with varying degrees of differentiation toward blood vessel endothelium. An alternative hypothesis for the histogenesis of Kaposi's sarcoma would be one of multicentric hyperplasia containing lymphatic venular anastamoses with elements of both lymphatic and blood vessel endothelium.
J Invest Dermatol 1989 Aug
PMID:Histogenesis of Kaposi's sarcoma and angiosarcoma of the face and the scalp. 266 17

We investigated the number and morphology of Langerhans' cells in the epidermal component of squamous cell carcinomas located on the sun-exposed skin of 10 patients. Using adenosine triphosphatase-stained epidermis from the tumors, we compared the Langerhans' cells in squamous cell carcinoma with those in nontumorous skin specimens from the same patient. The nontumorous skin specimen was obtained from either sun-exposed perilesional or non-sun-exposed sites. In three patients a normal number and almost normal morphology of Langerhans' cells were observed within the epidermal component of the tumor. One patient showed a normal number but a profound alteration of the morphology of the cells. In the remaining six patients, a significant decrease in the number of Langerhans' cells was observed. Langerhans' cells within the epidermal component of the tumors of these patients exhibited morphologic alterations in that they were mainly round or oval rather than highly dendritic. In none of our patients was the number of Langerhans' cells in the tumor increased. We conclude that a decreased number and altered morphology of Langerhans' cells occur in some, but not all, squamous cell carcinomas of the skin, and that there is no apparent difference between the number of Langerhans' cells in sun-exposed vs unexposed skin from the same individual.
Arch Dermatol 1989 Jul
PMID:Variations in the number and morphology of Langerhans' cells in the epidermal component of squamous cell carcinomas. 249 13

The effects on murine Langerhans cells (LC) of steroid and non-steroid immunosuppressive drugs which are commonly used for long-term immunotherapy of human patients were investigated. Hydrocortisone, prednisolone, cyclosporin A or azathioprine was administered daily for 7 consecutive days either topically by application to the skin, or systemically by intraperitoneal injection. LC densities were determined on the day following cessation of treatment by staining for the plasma membrane-bound enzyme adenosine triphosphatase (ATPase). All immunosuppressants caused a significant reduction in ATPase-positive LC when administered topically, but not systemically. The systemically administered drugs, although given in high concentration, may not have penetrated the epidermis in sufficient concentrations to disrupt the LC membrane. These observations are consistent with long term immunosuppressants depleting cutaneous LC by bone marrow suppression rather than by a direct effect on LC.
Br J Dermatol 1986 Jan
PMID:Reduction in murine Langerhans cell ATPase staining following topical but not systemic treatment with steroid and non-steroid immunosuppressants. 293 80

In the guinea pig, experimental allergic contact dermatitis (ACD) and primary irritant contact dermatitis (PICD) were induced with different concentrations of dinitrochlorobenzene (DNCB). The epidermal Langerhans' cells (LCs) were observed sequentially by both adenosine triphosphatase (ATPase) and electron microscopy. Light microscopically, in ACD, the density and dendritic processes of LC decreased markedly within 12 h after antigen challenge. Almost no recognization LCs could be seen within 2 to 5 days. Later, LCs began to repopulate in the epidermis. Within 14 days, the density and shape of the LCs returned to normal. On the contrary, LCs changed more rapidly in PICD. The dendritic processes of LC decreased within 2 h and cell density decreased dramatically within 6 h after DNCB application. LCs also repopulated more rapidly in the epidermis. Electron microscopically, in ACD, we observed that lymphocyte-like cells apposed to LCs; LCs were activated and damaged; however, in PICD, we found neither the apposition of lymphocyte-like cells to LCs, nor the activation of LCs. LCs play an important role in the convalescence phase as well as in the early and later phases of contact allergic reaction.
Int J Dermatol 1985 Dec
PMID:Cytochemical and ultrastructural studies of the Langerhans' cells. Sequential observations in experimental contact allergic reaction. 293 5


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