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)

Treatment with neuraminidase decreased the activity of Na+,K+-activated Mg2+-adenosine triphosphatase in plasma membranes isolated from experimental granulation tissue but not that of 5'-nucleotidase or leucine-beta-naphthylamidase. A temporary lowering of the pH of the plasma membrane suspension to 2-3 inactivated all three enzymes, which remained inactive after the pH had been readjusted to 7.4. Addition of dextran preparations to the membrane suspension decreased the activity of adenosine triphosphatase. Ethanol (0.4%) had a similar effect. These marker enzymes of plasma membranes were not affected by additions of hyaluronate, chondroitin sulfate, protein polysaccharide or soluble collagen. Serotonin stimulated the adenosine triphosphatase activity slightly. About 10-20% of the protein in the plasma membrane preparation was extracted with EDTA. This "fuzzy coat" fraction yielded a distinct gel-electrophoretic protein pattern. Hyaluronidase was not helpful in cleaving this surface layer from the plasma membranes.
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PMID:Properties of plasma membranes from granulation tissue with reference to extracellular matrix. 0 56

The biceps femoris muscle was surgically incised and sutured in 10 clinically healthy mongrel dogs, aged 1-2 yr and weighing 10-15 kg. The surgical wounds of 5 dogs were exposed to shortwave diathermy for 5 min daily for 7 days, starting a day after the creation of trauma. The remaining 5 dogs served as control. After 15 days of healing, the tissues from biceps femoris muscle were collected and subjected to histomorphological and histochemical examination. Mature collagen bundles were seen at healing site in diathermy treated animals while there were immature collagen fibres and more number of fibroblasts in control animals. Normal muscle fibres could be seen on either side of the healing tissue in treated animals whereas in control animals, atrophied and necrosed muscle fibres were encountered. The neutral and acid mucopolysaccharides, lipid droplets in the intermyofibrillar area and the activity of alkaline phosphatase, adenosine triphosphatase and lactate dehydrogenase at the healing site was better in treated as compared to controls.
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PMID:Histomorphochemical effects of shortwave diathermy on healing of experimental muscular injury in dogs. 225 71

An experimental model of myocardiopathy was induced in rhesus monkeys following noradrenaline (NA) infusion (20 ug/kg body wt/minute), for a period of 2 hours daily for three consecutive days. The animals were sacrificed after two hours (acute phase), forty-eight hours (sub-acute phase) and twenty-one days (chronic phase). Focal depletion of succinic dehydrogenase, increase in adenosine triphosphatase, acid phosphatase and appearance of large fat droplets in myocardial muscle was noted in the acute phase. Histopathological examination revealed focal edema, opacity and fuchsinorrhagia of the muscle fibres distributed in both the ventricles. Myofibrillar degeneration, myocytolysis and vacuolization with aggregation of lymphomononuclear cells were the significant features in the acute phase. During sub-acute and chronic phases, these features became less prominent and reparative changes with proliferation of fibroblasts became more marked. By the twenty-first day, irregular, focal scars replaced the necrosed myocardium. Ultrastructurally, heart muscle showed myofibrillar disorganisation, distortion of Z and A bands, dilatation of sarcoplasmic reticulum and swelling and rupture of mitochondria. Altered membrane permeability was evidenced by the presence of reaction products of horseradish peroxidase within the cardiac cells. In the reparative phase, however, myocytolytic changes regressed and collagen deposition was the prominent feature. This experimental study has several histological features simulating human cases of myocardial infarction without coronary occlusion.
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PMID:Catecholamine-induced experimental cardiomyopathy--a histopathological, histochemical and ultrastructural study. 259 40

Enzymatic activities of calcium-magnesium dependent adenosine triphosphatase (Ca-ATPase) and nonspecific alkaline phosphatase (ALPase) were localized at the initial calcification sites of dentin and enamel of rat incisor teeth using electron-microscopic cytochemistry. Ca-ATPase was localized in the Golgi cisternae, cytoplasmic vesicles and along the outer surface of the presecretory and secretory ameloblasts, whereas it was totally absent from the odontoblasts in the pulp. Inversely, ALPase reaction was localized along the outer surface of the odontoblasts, but almost completely absent from the ameloblasts. Diffuse extracellular reactions of both enzymes were distributed throughout the unmineralized fibrous matrix of mantle dentin in which a large number of matrix vesicles were scattered. Both Ca-ATPase and ALPase reactions, which appeared in the matrix vesicles in the process of formation of mantle dentin, became most conspicuous at the site of initial dentin calcification. At this stage, an intense Ca-ATPase reaction also appeared along some of the collagen fibrils adjacent to the reactive matrix vesicles. No ALPase reaction was localized along these Ca-ATPase reactive collagen fibrils. Our observations suggest strongly that Ca-ATPase in the matrix vesicles originates from the inner enamel epithelium and/or preameloblasts whereas ALPase originates from the odontoblasts in the pulp. The importance of the coexistence of both enzymes for the control of initial calcification of dental hard tissues is suggested.
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PMID:Ca-ATPase and ALPase activities at the initial calcification sites of dentin and enamel in the rat incisor. 293 60

Early atherosclerotic lesions in human aortas less than five hours postmortem were studied by light microscopy (20 cases) and electron microscopy (10 cases), to determine the morphological and cytochemical character of calcium deposition in the lesions. Routine and multiple special stains by light microscopy demonstrated atherosclerotic (intimal) calcium to be deposited as fine grains, ring-shaped droplets or small needle-shaped crystals, and medial calcium as fine grains or ring-shaped droplets. The calcium deposits were frequently associated with the PAS-positive basal lamina surrounding smooth muscle cells. In the intimal lesions the calcium deposits were often associated with fine granular lipid, while this association was much less frequent in the media. Calcium in atherosclerotic intima was generally not closely associated with elastic fibers but in the media was often deposited along or near elastic fibers. By electron microscopy the atherosclerotic lesions were composed of many smooth muscle cells (with or without lipid droplets), newly formed elastic fibers, amorphous ground substance, a few collagen fibrils and many membrane-limited matrix vesicle-like structures, 100-700 nm diameter. Many similar vesicles were present between the elastic laminae of the media. With the potassium pyroantimonate technique for demonstrating calcium, reaction products were most concentrated within these matrix vesicles but were also present in mitochondria of smooth muscle cells, within extracellular mitochondria-like structures, in pericellular basal lamina-like material and loosely dispersed in the interstitial ground substance. All elastic fibers were negative for calcium by this technique. The membrane of the matrix vesicle-like structures were cytochemically positive for alkaline phosphatase and adenosine triphosphatase. These studies suggest that calcification in human atherosclerosis and media is related to smooth muscle cell degeneration and that the major initial loci for calcium deposition are matrix vesicles from degraded cells, comparable to osteogenic calcification of cartilage.
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PMID:Calcification in atherosclerosis. I. Human studies. 294 18

The effects of aldosterone on transepithelial sodium transport (measured by the short-circuit current (SCC) and on Na+-K+-adenosine triphosphatase (ATPase) biogenesis have been studied in A6 kidney cells grown on collagen-coated filters in two different media. In medium A, base-line SCCA was close to zero but transmural electrical resistance (RA) was high. Aldosterone (100 nM, t24h) drastically increased SCCA and RA, but only after a 4-h latent period. In medium B, base-line SCCB and RB were significantly higher than in medium A. Aldosterone significantly enhanced SCCB and to a lesser extent RB after a much shorter latent period (approximately 45 min) than in medium A. In medium A, aldosterone elicited a fourfold increase in the relative rate of synthesis of alpha- and beta-subunits of Na+-K+-ATPase. A twofold increase was already observed within the observed latent period. This time course suggests that de novo synthesis of sodium pumps might be one of the critical factors underlying the increase in sodium transport in this growth medium. In medium B, aldosterone elicited a two- to fourfold increase in the relative rate of synthesis of the alpha- and beta-subunits of Na+-K+-ATPase that paralleled SCCB. Thus de novo synthesis of Na+-K+-ATPase is clearly not a prerequisite for the early mineralocorticoid response (t90 min - t180 min), but still could be part of the late mineralocorticoid response (t3 h - t24 h). In both media, the immunochemical cellular pool of Na+-K+-ATPase was apparently not modulated by aldosterone for up to 48 h of incubation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Aldosterone regulation of Na+ transport and Na+-K+-ATPase in A6 cells: role of growth conditions. 303 69

For comparison with our previous study on early calcification in human atherosclerosis, the aortas of rabbits and chickens with experimentally induced atherosclerosis were studied by gross examination, light microscopy and electron microscopy, including various cytochemical techniques. Nine male New Zealand white rabbits and nine male white leghorn chickens were fed an atherogenic diet of chow with 8% peanut oil and 2% cholesterol for one, two or three months. Six rabbits and six chickens, fed normal chow for one, two or three months, served as controls. The normal diet chickens were found to have lipid-negative spontaneous fibrous plaques in the abdominal aorta, which following atherogenic diet developed lipid deposition and increasing calcium deposition. The normal diet rabbits had no aortic lesions, but following an atherogenic diet developed highly lipid-positive foam cell intimal lesions which subsequently developed increasing amounts of smooth muscle cells and calcium. Ultrastructurally, the aortic plaques in normal diet chickens were composed of smooth muscle cells, collagen, elastic fibers, ground substance and a few small extracellular matrix vesicles bounded by a trilaminar membrane. In the atherogenic diet chickens, these vesicles increased in number as did their staining for calcium by the pyroantimonate technique. The membranes of vesicles were cytochemically positive for alkaline phosphatase and adenosine triphosphatase. Similar matrix vesicles were present in the interstitium of the media. In both intima and media, the vesicles appeared to be largely derived from degenerating smooth muscle cells. The aortas of atherogenic diet rabbits were similar to the chickens except for many more lipid-laden foam cells.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcification in atherosclerosis. II. Animal studies. 378 82

To study the mechanism of LH-releasing hormone (LHRH) pulse generation, the olfactory pit/placode and the migratory pathway of LHRH neurons from monkey embryos at embryonic age 35-37 were dissected out, under the microscope, and cultured on plastic coverslips coated with collagen in a defined medium for 2-5 weeks. First, we examined whether cultured neurons release the decapeptide into media. It was found that LHRH cells release LHRH in a pulsatile manner at approximately 50-min intervals. Further, LHRH release was stimulated by depolarization with high K+ and the Na+ channel opener, veratridine. However, whereas the Na+ channel blocker, tetrodotoxin suppressed the effects of veratridine, tetrodotoxin did not alter the effects of high K+. Subsequently, the role of extracellular and intracellular Ca2+ in LHRH release was examined. The results are summarized as follows: 1) exposing the cells to a low Ca2+ (20 nM) buffer solution suppressed LHRH release, whereas exposure to a normal Ca2+ solution (1.25 mM) maintained pulsatile LHRH release; 2) LHRH release from cultured LHRH cells was stimulated by the voltage-sensitive L-type Ca2+ channel agonist, Bay K 8644 (10 microM), whereas it was suppressed by the L-type Ca2+ channel blocker, nifedipine (1 microM), but not by the N-type channel blocker, omega-conotoxin GVIA (1 microM); 3) the intracellular Ca2+ stimulant, ryanodine (1 microM), stimulated LHRH release, whereas the intracellular Ca2+ transporting adenosine triphosphatase antagonist, thapsigargin (1 and 10 microM), did not yield consistent results; and 4) carbonyl cyanide p-trifluoromethoxyphenyl-hydrazone (1 microM), a mitochondrial Ca2+ mobilizer, stimulated LHRH release, whereas ruthenium red, a mitochondrial Ca2+ uptake inhibitor, did not induce consistent results. These results indicate that: 1) the presence of extracellular Ca2+ is essential for LHRH neurosecretion; 2) Ca2+ enters the cell via L-type channels but not N-type channels; and 3) mobilization of intracellular Ca2+ from inositol 1,4,5-triphosphate-sensitive stores, as well as mitochondrial stores, seem to contribute to LHRH release in these cells.
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PMID:Pulsatile release of luteinizing hormone-releasing hormone (LHRH) in cultured LHRH neurons derived from the embryonic olfactory placode of the rhesus monkey. 1006 21

Homozygous mutant klotho (KL(-/-)) mice exhibit multiple phenotypes resembling human aging. In the present study, we focused on examining the pathology of the lungs of klotho mice and found that it closely resembled pulmonary emphysema in humans both histologically and functionally. Histology of the lung of KL(-/-) mice was indistinguishable from those of wild-type littermates up to 2 wk of age. The first histologic changes appeared at 4 wk of age, showing enlargement of the air spaces accompanied by destruction of the alveolar walls, and progressed gradually with age. In addition to these changes, we observed calcium deposits in type I collagen fibers in alveolar septa and degeneration of type II pneumocytes in 8- to 10-wk-old KL(-/-) mice. Pulmonary function tests revealed prolonged expiration time in KL(-/-) mice, which is comparable with the pathophysiology of pulmonary emphysema. The expression level of messenger RNA for type IV collagen, surfactant protein-A and mitochondrial beta-adenosine triphosphatase was significantly increased in KL(-/-) mice, which may represent a compensatory response to alveolar destruction. Additionally, the heterozygous mutant klotho mice also developed pulmonary emphysema late in life, around 120 wk of age. These findings indicate that klotho gene expression is essential to maintaining pulmonary integrity during postnatal life. The klotho mutant mouse is a useful laboratory animal model for examining the relationship between aging and pulmonary emphysema.
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PMID:Disruption of the klotho gene causes pulmonary emphysema in mice. Defect in maintenance of pulmonary integrity during postnatal life. 1061 62

To study the histochemical alterations of hookworm L3 administered in a challenge dose to mice vaccinated previously with the larvae. Male Kunming strain mice vaccinated subcutaneously with 500 living Ancylostoma caninum L3 once every 2 weeks for a total of three immunizations before a final challenge with 500 L3 one week after the final immunization. The abdominal skin with underlying subcutaneous tissue and muscle were removed from the site of percutaneous challenge entry (from 2-3 mice), and fixed in absolute alcohol, cold acetone and 10% neutralized formalin. The tissue sections containing the L3 from the challenge dose were then stained histochemically of glycogen, RNA, DNA alkaline protein, acid mucopolysaccharide, collagen, reticulin, alkaline phosphatase (AKP) and adenosine triphosphatase (ATPase). Skin samples from non-immunized mice that were also subcutaneously inoculated with the L3 served as negative control. The L3 identified in cutaneous sections from vaccinated mice at 6-72 hours post-challenge exhibited reductions in parasite glycogen, alkaline protein, RNA and DNA, as well as reductions in acid mucopolysaccharide, collagen and reticulin contents in the parasite cuticle. There were also reduced enzyme AKP and ATPase activities. In contrast L3, identified in sections from non-immunized mice exhibited a normal histochemical appearance, as did some L3 who survived in vaccinated mice at 7-14 days post-challenge. Vaccination results in hookworm L3 damage which is manifested by reduced histochemical staining for the challenge inoculum of parasites. There is also reduced hydrolytic enzyme activity. The observed changes could reflect either host-mediated parasite structural damage and disintegration or possibly anti-metabolic properties of the host immune response.
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PMID:Histochemical alterations of infective third-stage hookworm larvae (L3) in vaccinated mice. 1077 9


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