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)

Sheets of ethylenediaminetetraacetic acid (EDTA)-separated epidermis were examined using scanning electron, transmission electron, and light microscopy; sheets were also examined after staining for adenosine triphosphatase (ATPase) activity. Staining was improved by longer incubation with EDTA and by elimination of Trismal buffer as a tissue rinse. EDTA-separated epidermis showed better retention of ultrastructural integrity when washed with phosphate-buffered saline. The ATPase staining procedures described in this present study are ultrastructurally specific for the Langerhans cell.
J Invest Dermatol 1983 Feb
PMID:EDTA separation and ATPase Langerhans cell staining in the mouse epidermis. 621 8

It has been postulated that a relationship exists between the density of epidermal Langerhans cells and the capacity of the epidermis to promote the induction of contact sensitization. This postulate was developed, in part, because (1) mouse tail epidermis contains fewer ATPase-positive (presumably Langerhans) cells than does abdominal epidermis, and (2) when tails of C57Bl/6 mice were painted with dinitrofluorobenzene (DNFB), the mice were less sensitive than those painted on the abdomen. In addition, tail-painted mice were shown to be tolerant to subsequent attempts at sensitization with DNFB. In this study we found that by painting the tails of mice with the hapten trinitrochlorobenzene (TNCB), sensitization was induced in certain mouse strains (BALB/c, A/J, and CBA--haplotypes H-2d, H-2a, H-2k, respectively), but tolerance resulted from painting the tails of other strains (C57Bl/6, C57Bl/10, and AB.Y--haplotype H-2b). The ability to become sensitive or tolerant is not related to Langerhans cell density as detected by ATPase staining. While the mechanism for this strain difference in the induction of tolerance is unknown, tolerance induced in C57Bl/6 mice is mediated in part by the generation of suppressor cells.
J Invest Dermatol 1983 May
PMID:Strain variation in the induction of tolerance by epicutaneous application of trinitrochlorobenzene. 622 Oct 52

Epidermal Langerhans cells (LC) disappear during photochemotherapy (PUVA) with 8-methoxypsoralen (8-MOP) and long wavelength ultraviolet (UV-A) radiation. The time course of their disappearance during treatment and their reappearance after its completion was followed. Langerhans cells lost ATPase activity before they disappeared by ultrastructural criteria: thus 90% of ATPase-stained cells had disappeared after seven treatments (2 weeks) whereas it was only after fifteen treatments (5 weeks) that they were seen to be reduced on electron microscopy. Their numbers remained low throughout the course of treatment but they had returned to normal by 3 weeks after cessation of therapy. Since PUVA lamps also emit traces of medium wavelength UV (UV-B) the separate effects of UV-A and UV-B in the presence and absence of 8-MOP were examined. Within the dose range normally used for therapy, the LC disappeared only with the combination of UV-A and 8-MOP.
Br J Dermatol 1983 Sep
PMID:Reappearance of epidermal Langerhans cells after PUVA therapy. 622 52

We have investigated the effect of ultraviolet-B (UVB) irradiation on the density of epidermal ATPase-positive Langerhans cells, and the modulation of this effect by indomethacin (IND). Depilated backs of albino guinea pigs were exposed to varying doses of UVB (10-550 mJ/cm2). Skin biopsies were taken serially. There was an UVB dose-dependent decrease in the density of dendritic epidermal Langerhans cells, as identified by their membrane ATPase activity. This was accompanied by thinning and shortening, or disappearance of dendritic processes. Such changes were followed by a gradual recovery of the cell density to preirradiation level by day 21. Despite the high doses of UVB given, the maximal decrease in the density of ATPase-positive cells was only 58%. Topical application of IND, a prostaglandin-synthetase inhibitor, after irradiation resulted in a decrease of the erythema; however, the decrease in the density of ATPase-positive cells was still observed. In contrast, guinea pigs that received IND topically prior to irradiation showed a decrease erythemal response, but failed to show any decrease in the density of ATPase-positive cells. Administration of IND orally for 3 days prior to UVB exposure did not prevent the decrease in the cell density. The protective effect of topical IND, applied prior to irradiation, may be explained by its in vitro absorbance at both the UVB and UVA ranges. Topical application of IND 20 min prior to exposure to UVB in 2 human subjects resulted in an increase in the minimal erythema dose, giving a sun protection factor of 1.6, which is comparable to that produced by an equimolar concentration of para-aminobenzoic acid solution. The sun-protective property of IND, together with its activity as a prostaglandin synthetase inhibitor, indicate that it potentially could be a useful sunscreen agent. Its clinical safety and efficacy, however, remain to be determined.
J Invest Dermatol 1983 Nov
PMID:Effect of indomethacin on alteration of ATPase-positive Langerhans cell density and cutaneous sunburn reaction induced by ultraviolet-B radiation. 622 48

Modified ATPase histochemistry was used to identify and count Langerhans cells (LC) in autopsy tissue from 8 oral mucosal sites, 8-20 h postmortem. The specificity of the ATPase method was confirmed on serial sections with indirect immunofluorescence using monoclonal antibodies OKT6 and antihuman Ia. Average LC counts on ATPase-stained epithelial sheets from each of the 8 sites ranged from 160-550 LC/mm2. Nonkeratinized mucosae of the soft palate, ventral tongue, lip, and floor of the mouth had the highest counts (mean +/- SD, 508 +/- 110 LC/mm2, n = 24), and keratinized mucosae of the hard palate and gingiva had the lowest counts (201 +/- 97 LC/mm2; n = 8). LC frequency was variable in 2 sites: In the dorsal tongue, LC occurred on only one side of filiform papillae and were absent from regularly recurring areas of interpapillary epithelium. In the cheek mucosa, LC clustered around connective tissue papillae and their numbers showed marked individual variation (130-650 LC/mm2). The number of LC in nonkeratinized oral mucosa is approximately the same as in skin, but keratinized oral mucosa has fewer LC. The frequency of oral mucosal LC varies inversely with the degree of keratinization. There are regions of the oral mucosa that have no LC.
J Invest Dermatol 1984 Jan
PMID:Human mucosal Langerhans cells: postmortem identification of regional variations in oral mucosa. 622 11

The effect of 750 rads of gamma radiation on the rate of return of epidermal Langerhans cells (LC) following suppressive doses of topical glucorticoids was studied in guinea pigs. Gamma radiation alone had no effect on the LC as assessed by staining for cell membrane ATPase activity and Ia antigen. It did, however, delay the expected return of Ia but not ATPase surface markers on the LC after perturbation with glucocorticoids. The delayed return of surface Ia antigen is possibly related to a radiation-induced defect in the production of a required lymphokine and/or in intracellular Ia transport. Although our data do not rule out a cytolytic effect of steroids on the LC, they do strongly suggest that, at least in part, glucocorticoids act on the LC by altering cell surface characteristics.
J Invest Dermatol 1984 Feb
PMID:Effect of glucocorticoids and gamma radiation on epidermal Langerhans cells. 622 85

Unlike keratinocytes, Langerhans cells express both surface ATPase activity and Ia (HLA-DR) antigens. A well-characterized in vitro system containing Langerhans cells would be of great use in elucidating their functions. Thus, epidermal cell cultures derived from neonatal Balb/c mice were examined for the presence of Langerhans cells. Twenty-four hours after initiation of culture, ATPase- and Ia-positive cells were seen to be associated with cell aggregates. By day 3, Langerhans cells migrated on to the substratum and, as the cultures matured and stratified, were seen both in groups and as single cells for the duration of the cultures (day 14). During culture, although the total number of cells increased, the percentage of cells expressing Ia antigen and ATPase activity remained constant, suggesting that Langerhans cells increase in number during cell culture. Such a situation could arise from actual division of Langerhans cells during culture or from latent expression of Ia antigen and ATPase activity by pre-existing cells. This is the first study of the dynamics of Langerhans cells in a cell culture system and shows that Langerhans cells are present throughout the lifespan of the cultures.
Br J Dermatol 1984 Mar
PMID:Dynamics of Langerhans cells in genetically defined murine epidermal cell culture. 623 98

A great deal of knowledge has been gained concerning the activation of adenylate and guanylate cyclase in epidermal cells. Adenylate cyclase is activated by 4 different independent receptors-responding respectively to catecholamine (beta), to prostaglandins (E), to histamine (H2), and to adenosine and it phosphorylated derivatives. Upon activation, each of these receptors becomes unresponsive to further stimulation by its specific stimulator. Guanylate cyclase, on the other hand, is activated by histamine (H1) and epidermal growth factor (EGF). Unlike EGF, the histamine activation is extremely rapid (less than 5 minutes). Epidermal cells are permeable (leak) to cyclic GMP but not cyclic AMP. When the skin is traumatized or injured in any way (even by intradermal injection) there is a sudden catastrophic change in the intracellular levels of the cyclic nucleotides (and of ATP). Cyclic AMP rapidly rises to perhaps 5-10 times its normal resting level while cyclic GMP falls to 10-20% of its level in vivo. The rise in cyclic AMP is due to activation of adenylate cyclase while the fall in cyclic GMP is due in major part to activation of cyclic GMP phosphodiesterase (and perhaps the fall in ATP is due to activation of ATPase). The changes in ATP and cyclic AMP can be reversed by incubating the tissue in a buffered salt solution containing glucose, but this does not normalize the cyclic GMP content. The fall in cyclic GMP can be prevented by a phosphodiesterase inhibitor (IBMX ). This series of events has been called the "ischemia effect." However, it implies that a lack of oxygen is at fault, and that has not been shown to be the case. Its underlying cause and possible physiologic significance are not known. Do these changes in cyclic nucleotides have effects on epidermal proliferation? And does EGF? Agents which increase cyclic AMP do inhibit the epidermal outgrowth and mitotic activity of explant cultures of pig skin. Cyclic GMP does increase outgrowth at a particular concentration. Histamine, which elevates both cyclic nucleotides, has a biphasic action depending on its concentration. These findings imply that these nucleotides do act as one of the controls of epidermal proliferation. The action of cyclic GMP is not accompanied by detectably increased phosphorylation of epidermal proteins. On the other hand, EGF action which also enhances epidermal outgrowth is characterized by an increased protein phosphorylation that precedes any increase in cellular cyclic GMP. We conclude that the action of EGF is independent of the cyclic nucleotide system.
Curr Probl Dermatol 1980
PMID:Cyclic GMP system in the epidermis. 626 50

Glucocorticoids are known to influence DNA and RNA synthesis in skin fibroblasts. In a novel approach to study this effect, we investigated the influence of the hormone analogue dexamethasone on the activity of nuclear envelope-associated nucleoside triphosphatase (NTPase) in intact cell systems (3T3 fibroblasts and MMLI melanoma cells). The NTPase is thought to be responsible for regulation of nucleocytoplasmic transport of mRNA. [3H]Dexamethasone was found to bind to nuclear ghosts at a density comparable with that of nuclear pores in this cellular fraction. Incubation of the cells for 48 h in the presence of different concentrations of dexamethasone resulted in a marked decrease of NTPase activity. Already concentrations as low as 0.1 ng/ml (3T3) or 1 ng/ml (MMLI) reduced the NTPase activity by approximately 50%. These results suggest that nuclear envelope NTPase is a site at which glucocorticoids regulate gene expression.
J Invest Dermatol 1984 Jul
PMID:Effect of dexamethasone on nuclear envelope nucleoside triphosphatase in fibroblasts 3T3 and melanoma cells MMLI. 633 Feb 11

In vivo studies have demonstrated that various treatments of skin, e.g., UV irradiation, topical corticosteroids, and tape-stripping, will temporarily deplete the epidermis of Langerhans cells (LC). Whether this loss represents simply a loss of cell surface markers unique to LC, or actual depletion of cells, is unknown. By design, normal human skin transplanted to the congenitally athymic (nude) mouse is a system devoid of circulating precursors for human LC. Because LC have been shown to be of bone marrow origin, any depletion of these cells in this system should be permanent. Treatments to deplete LC from human skin grafts on nude mice after grafting included: (a) large doses of UV radiation (400 mJ/cm2 every 48 h, X 3), (b) potent high-dose topical corticosteroids (2.5 mg betamethasone valerate/cm2 every day, X 5), (c) tape-stripping (X 20). Treatments before grafting included: (a) treating donor skin with 900 R of gamma irradiation, (b) complement fixing monoclonal antibody to Ia-like antigens of LC, followed by fresh complement, (c) monoclonal antibody conjugated to toxins. Quantitation of the number of LC was analyzed on control and treated epidermal sheets using immunodiagnostic reagents, anti-HLA-DR, and surface ectoenzymes , ATPase. Results show that both UV irradiation and topical corticosteroids reduce the number of LC by these analyses. However, within 3 weeks, recovery to pretreatment levels has occurred. X-irradiation and tape-stripping were without effect. Despite evidence that the monoclonal antibody, complement, and toxic systems were delivered to the LC within the epidermis, there is no evidence that these treatments resulted in a decrease in LC. It appears that LC are currently either long-lived or replaced locally from a proliferative pool and that certain cell membrane determinants of human LC are somewhat differentially sensitive to UV radiation and corticosteroids.
J Invest Dermatol 1984 Jun
PMID:Biology of Langerhans cells: analysis by experiments to deplete Langerhans cells from human skin. 637 58


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