Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.6.1.3 (ATPase)
 65,361 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A technique which enables good visualization of the membranous ATPase activity of epidermal Langerhans cells is described. The method has the advantage of keeping intact most of the ultrastructural details. It may allow the observation, under pathologic conditions, of ultrastructural modifications in ATPase-negative Langerhans cells still recognizable by their Langerhans cell granules.
J Invest Dermatol 1986 Jan
PMID:ATPase Langerhans cell staining: a technique allowing progression from light to electron microscope observation. 242 94

Langerhans cells (LCs) have been identified in human skin by 10 weeks estimated gestational age (EGA), but it was not known when they first enter the epidermis or acquire HLA-DR, OKT-6, and ATPase reactivity. We assayed for LCs in human embryonic and fetal skin by using immunolabeling and histochemical techniques on epidermal sheets. HLA-DR+ and ATPase+ LCs were present in the epidermis by 6-7 weeks EGA, the youngest tissue examined. Most LCs were OKT-6- until about 12 weeks EGA when they underwent a dramatic increase in OKT-6 reactivity. Although LC densities between 50-100 days were statistically similar (100 cells/mm2 of epidermis), LCs early in development were smaller, less dendritic, and phenotypically heterogeneous. We conclude that LCs migrate into the epidermis during the first trimester and resemble the adult phenotype by the second trimester, long before the immune system is fully activated.
J Invest Dermatol 1986 Mar
PMID:Ontogeny of Langerhans cells in human embryonic and fetal skin: expression of HLA-DR and OKT-6 determinants. 242 3

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

We have previously reported a sequence of events which occurs during the recovery phase of the murine epidermal Langerhans cells (ELCs) after ultraviolet-B irradiation. We found that an ATPase-positive round cell divides, dendrites are gradually formed, and paired dendritic cells are eventually separated as the post-irradiation time elapses. We wondered if a series of events similar to this might occur in the normal murine epidermis without irradiation. In this study, we could identify exactly the same phases of the ELC mitotic cycle in normal mouse ear skin.
J Invest Dermatol 1989 Jan
PMID:Mitotic activities of normal epidermal Langerhans cells. 252 Dec 38

We have previously described an ATPase Langerhans cell (LC) staining technique allowing progression from light to electron microscope observation. Using this technique we have studied, following epicutaneous application of a sensitizing dose of a hapten, 2,4-dinitro-1-fluorobenzene (DNFB), the fate of the epidermal LC located in the sensitization zone. We wanted to know, under the light microscope, if the density and/or morphology of the LC are modified by such a treatment and, under the electron microscope, what are the ultrastructural changes accompanying the possible light microscope modifications. Under the light microscope, the observation of LC during the 5 d necessary for the development of contact sensitivity to DNFB shows that their number drops in the course of the first 24 h to normalize again 3 d later. Under the electron microscope, observations over the first 24 h revealed that LC remained in the epidermis, but were ATPase-negative. The disappearance of the membrane ATPase activity took place while the LC presented an increased number of coated pits, coated vesicles, endosomes, and lysosome organelles which characterize, at the ultrastructural level, the process of receptor-mediated endocytosis (RME). Following RME, many Birbeck granules (BG) appeared in the cytoplasm. Thus, epicutaneous application of DNFB leads to an endocytic activation of LC. However, the ligand(s) and/or the cell-surface components, which probably internalize during the RME process, remain unknown.
J Invest Dermatol 1989 May
PMID:ATPase and morphologic changes in Langerhans cells induced by epicutaneous application of a sensitizing dose of DNFB. 252 42

Electron-microscopic and ultra-cytochemical studies have shown the structural and functional features of pyoderma agents--staphylococci isolated from patients with acute and chronic pyoderma. The studies have revealed magnesium-activated ATPase and adenylate cyclase in these bacteria; the authors have tried to trace a correlation between these enzymes' activities and location and the disease pattern. This may help assess the bacterial population status and choose the drugs for purposeful pathogenetic therapy.
Vestn Dermatol Venerol 1989
PMID:[Structuro-functional properties of staphylococci in patients with pyoderma]. 252 50

Epidermal Langerhans cells (ELC) are bone marrow-derived immune cells that are important in allergic contact dermatitis. We examined the influence of calcium transport inhibitors, lanthanum and diltiazem hydrochloride, on allergic contact dermatitis induced by 1-chloro-2,4-dinitrobenzene (DNCB) in BALB/c mice. Systemic lanthanum at a dose of 0.08 mg/kg and topical lanthanum (50 microliters of 10% solution) were given 5 d before DNCB sensitization. Systemic diltiazem (30 mg/kg per dy) was given for 3 d during sensitization with DNCB. In all animals, challenge with topical DNCB to the ear skin was performed 5 d after sensitization and ear swelling was measured. Twenty four hours post-DNCB challenge, animals receiving systemic lanthanum demonstrated a 56% decrease in contact hypersensitivity (ear swelling) compared with non-lanthanum-treated animals (0.08 +/- 0.03 mm vs 0.18 mm +/- 0.02 mm, p less than 0.01). Topical lanthanum produced a 58% decrease in contact hypersensitivity (0.20 +/- 0.02 mm vs 0.41 +/- 0.03 mm, p less than 0.01). The DNCB-induced ear swelling also resolved more quickly in animals treated with lanthanum. Systemic diltiazem produced a 67% decrease in ear swelling (0.05 +/- 0.01 mm vs 0.15 +/- 0.02 mm, p less than 0.001). A decrease in epidermal Langerhans cell density of 13 to 14% was produced by systemic lanthanum, detected by both ATPase staining and Ia staining, respectively (p less than 0.05). Approximately 20% of the Langerhans cells were morphologically abnormal, having become "rounded," and lacking normal dendritic processes. From these results, we infer that calcium transport across the cell membrane of ELC may be important in the regulation of their function. Lanthanides and other calcium-channel blockers may be useful pharmacologic agents to probe these phenomena.
J Invest Dermatol 1989 Sep
PMID:Inhibition of cutaneous contact hypersensitivity by calcium transport inhibitors lanthanum and diltiazem. 252 9

The effect of ultraviolet light-B (UVB) irradiation on the activity of prostaglandin (PG) D synthetase was investigated in adult rat skin. Rats were irradiated with 500 mJ/cm2 of UVB, and PGD synthetase activity was determined in 100,000 g supernatant of the homogenate of rat skin in the presence of glutathione (GSH) before and 3, 6, 12, and 24 h after irradiation. The PGD synthetase activity was decreased time dependently, and within 24 h after UVB irradiation it had dropped to 50% of the control level before irradiation. In contrast, the synthesizing activities of PGE2 and PGF2 alpha were unaffected by UVB irradiation. The reduction of PGD synthetase activity after UVB irradiation was much more prominent in the epidermis than in the dermis, which was separated by heat treatment (55 degrees C, 30 sec). Immunohistochemical studies, using anti-(rat spleen PGD synthetase) antibody, revealed that the number of immunopositive cells, which were identified as Langerhans cells, decreased in the basal layer of the epidermis 24 h after UVB irradiation. These results, together with the reduction of ATPase positive cells in the epidermis after UVB irradiation, suggest that the decrease of PGD synthetase activity in rat skin by UVB irradiation is, at least in part, due to the reduced Langerhans cell population in the basal layer of the epidermis.
J Invest Dermatol 1989 Sep
PMID:Effect of ultraviolet irradiation on the activity of rat skin prostaglandin D synthetase. 252 10

Electron spin resonance spectroscopy using the spin probe (5-, 12- and 16-deoxylstearic acid) was employed to analyze the changes in membrane fluidity in B-16 melanoma cells following UV-B exposure. The UV exposure resulted in the immediate accumulation of lipid peroxide, being accompanied by a change in membrane fluidity. The 12-DSA is the most sensitive to the changes in membrane organization caused by UV light. Na+,K+-ATPase activity was regulated by a change in membrane fluidity. Following UV exposure, the release of the prelabeled arachidonic acid from the cells was observed immediately. Ca2+-dependent calmodulin-dependent phospholipase A2-like activity was involved in the UV-stimulated arachidonic acid release from phospholipid.
Arch Dermatol Res 1989
PMID:Membrane responses of B-16 melanoma cells to single exposure to ultraviolet light. 253 9


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