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)

Modern biology provides satisfactory explanations for the abnormalities of the different phases of relaxation and diastole. Ventricular filling depends on three factors: active relaxation; the only factor is the concentration of ATP which has to re-increase. This requires elimination of the cytoplasmic calcium which activates ATP-ase by the Ca2+ ATPase of the sarcoplasmic reticulum and the Na+/Ca2+ pump. In hypertrophy, the concentration of the first and the activity of the second are decreased; passive wall compliance, which depends on the quantity and quality of parietal collagen. This factor is partially regulated in the myocardium by the concentration of aldosterone and angiotensin II; atrial contraction, which depends on the size of the atria and their isomyosine content. This changes in atrial overload to a slow form of myosine, one of the mechanisms of adaptation.
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PMID:[Biologist's view on diastolic dysfunction]. 183 66

PGE2 production by glomeruli is increased in a variety of glomerular diseases. Potentially, this process may affect mesangial cell protein synthesis and mesangial cell growth. Thus studies have been undertaken, using cultured human mesangial cells, to assess the effects of PGE2 on proline uptake, protein synthesis and cell proliferation. In the presence of 140 mM NaCl, incubation of mesangial cells with 0.01 to 1 microM PGE2 for 72 hours resulted in a marked decrease of 14C proline uptake, but did not modify 14C leucine uptake. Substitution of choline to sodium inhibited 14C proline uptake by 85% which became independent of PGE2, indicating that this PG specifically altered sodium-dependent proline uptake. Inhibition of this component reached 35 to 50% with 1 microM PGE2. The inhibitory effect of PGE2 on sodium-dependent proline uptake required a lag time of 48 hours, and was suppressed by ouabain, an inhibitor of Na+, K+ ATPase activity. PGE2 did not modify the Vmax of the transport system (1.007 vs. 1.023 nmol/mg/min) but increased (P less than 0.01) its Km (1.179 vs. 0.823 mM). 8-bromo-cyclic AMP also inhibited sodium-independent proline uptake, and PGE2 markedly increased cyclic AMP production. Taken together, these results suggested that PGE2 acted via cyclic AMP stimulation. PGE2 under identical conditions (1 microM, 72 hr incubation) produced a decrease in collagen synthesis estimated by the relative rate of collagen production after incubation of mesangial cells with 14C proline (percentage of 14C radioactivity in collagenase-sensitive proteins over total proteins). PGE2 also diminished the intracellular free proline pool. More generally, PGE2 inhibited cell proliferation and cell total proteins.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of prostaglandin E2 on proline uptake and protein synthesis by cultured human mesangial cells. 196 49

We now have a biological explanation for most of the physiological characteristics of the hypertrophied chronically overloaded heart: (i) the slowing of the active relaxation is, at least in part, explained by a diminished density in the Ca2+ ATPase of SR, a majority of the modifications in passive myocardial compliance are due to an enhanced collagen density and the diminution of the atrial contribution to ventricular filling is certainly a consequence of an isomyosin change in this particular tissue. (ii) The systolic dysfunction reflects, in fact, one of the most essential parts of the adaptational process, the slowing of Vmax. In human, this diminution is a consequence of a rather complex change in the expression of various genes coding for proteins responsible for myoplasmic calcium transient. (iii) Arrhythmogenecity, a well-known detrimental property of the hypertrophied heart, reflects the fragility of calcium homeostasis in this type of cell, and this fragility is likely to be a direct consequence of the rearrangement of the membrane proteins.
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PMID:The biological basis of modified myocardial function in hypertensive cardiopathy. 204 64

The levels of mRNAs encoding the alpha 1 chain of collagen IV and the B1 chain of laminin were assayed in the lenses and retinas of long-term (28-week) diabetic and galactosaemic rats in order to gain some insight into the effects on basement membrane (BM) synthesis in these tissues. mRNAs coding for beta-actin, glucose transporter protein and the alpha 2 catalytic subunit of Na+,K(+)-ATPase were also assayed to determine whether any effects on BM-coding mRNA levels were specific. Long-term diabetes had no significant effect on the levels of alpha 1 (IV) collagen mRNA but caused a significant reduction in the laminin B1 message in the lens. In the same samples, the level of the glucose transporter protein mRNA was found to be elevated significantly in the diabetic tissue, whereas the mRNAsen coding beta-actin and alpha 2 Na+,K(+)-ATPase were unaffected in comparison with age-matched controls. Long-term galactosaemia resulted in significant increases in the levels of all mRNAs assayed when expressed per micrograms total RNA used for each analysis. However, this effect appeared to be due to a specific loss of ribosomal RNA from these severely cataractous lenses. When related to the beta-actin mRNA internal control, the levels of mRNA in the galactosaemic lenses were very similar to that found in the diabetics. Laminin B1 mRNA levels were decreased significantly.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effects of long-term diabetes and galactosaemia upon lens and retinal mRNA levels in the rat. 216 48

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

The development of cell polarity in Madin-Darby canine kidney (MDCK) cells has been analyzed under conditions in which cells are induced to form multicellular epithelial cysts in stages that mimic the ontogeny of epithelial tissues and organs in vivo. The morphogenesis of MDCK cysts in suspension culture or in a collagen gel proceeds in distinct stages involving the initial aggregation of cells followed by development of a closed monolayer of polarized epithelial cells that surrounds a central lumen. The polarity of cells was determined at each stage by analyzing the distributions of marker proteins of the apical (gp135) and basal-lateral (Na+,K(+)-ATPase) domains of the plasma membrane, the tight junction (ZO-1) and proteins involved in cell-cell (uvomorulin) and cell-substratum contact (type IV collagen). We show that cells have a distinctive and opposite polarity in cysts formed in suspension culture compared to those formed in collagen gels. In suspension culture, the basal-lateral membrane faces the central lumen and the apical membrane faces the outside, whereas in collagen gel, the basal-lateral membrane faces the outside collagen and the apical membrane faces the central lumen. Detailed analysis of the distributions of marker proteins during the morphogenesis of these three-dimensional structures indicates that: (1) cell-cell contact is sufficient to trigger the segregation of marker proteins of the apical and basal-lateral membrane domains to distinct regions of the membrane; (2) cell-cell contact induces association of the tight junction protein ZO-1 with the contact zone between cells; (3) localization of the tight junction protein ZO-1 to the apex of the lateral membrane and the establishment of the epithelial axis, however, requires the formation of a basal lamina and cell-substratum contact; (4) in suspension culture, MDCK cysts secrete and establish a basal lamina in the central lumen. These results show that cell-cell and cell-substratum contact have distinct roles in the morphogenesis of polarized epithelia. We suggest that the mechanisms involved in triggering cell polarity may be common to different polarized epithelia in vivo.
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PMID:Steps in the morphogenesis of a polarized epithelium. I. Uncoupling the roles of cell-cell and cell-substratum contact in establishing plasma membrane polarity in multicellular epithelial (MDCK) cysts. 235 99

Human polycystic kidney disease (PKD) epithelia were successfully grown in culture and expressed abnormal characteristics. Cysts lining epithelia of superficial and deep cysts were microdissected and compared to individual normal human proximal straight tubules (PST) and cortical collecting tubules (CCT) grown in defined media. PKD cyst epithelia differed from normal renal tubular epithelia in growth patterns and structural and functional properties. PKD epithelia grew more rapidly and showed cyst-like areas in otherwise confluent monolayers. Polygonal and elongate cells contained an epithelial-specific cytokeratin antigen and had polarized morphology. An extremely abnormal basement membrane morphology was seen and consisted of some banded collagen and numerous unique blebs or spheroids. These blebs were apparently extruded from intracellular vacuoles and stained with ruthenium red, suggesting a proteoglycan component. Cytochemistry of marker enzymes demonstrated the presence of NaK-ATPase and alkaline phosphatase, but a lack of gamma-glutamyl transpeptidase. The response of adenylate cyclase activity to vasopressin, parathyroid hormone, and forskolin was significantly diminished in PKD cells as compared to PST and CCT. These studies suggest a defect in cell growth and basement membrane synthesis in human PKD. Cultured PKD epithelia provide a new tool for the study of the pathogenesis of this disease.
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PMID:A new method for studying human polycystic kidney disease epithelia in culture. 243 Nov 89

A subepithelial multilayer of abundant fusiform cells has been distinguished cytochemically in the urinary bladder and ureter in mice and rats. These distinctive cells stained selectively for carbonic anhydrase (CA) isozymes I and III. Immunonegativity for keratin and Na+,K+-ATPase differentiated the CA-positive cells from epithelial cells and their lack of immunoreactivity for actin distinguished them from smooth muscle cells. Immunostaining for vimentin, blue staining with the trichrome method, location in an exceptionally dense collagen stroma, and ultrastructural appearance related the multilayer cells to fibroblasts. A loosely collagenous, less cellular lamina propria separated the CA-positive suburothelial zone from the smooth muscle wall in the rodent urinary bladder. Ureter lacked the loose lamina propria, and the presence of such a collageneous layer in bladder therefore correlated with distensability of the organ. The presence of CA uniquely in the fibroblastoid cells applied intimately to ureter and bladder epithelium implies a specialized function of these cells, possibly one concerned with the barrier between blood and hypertonic urine. Cytochemical demonstration of keratin and fucose-rich glycoconjugate in the plasmalemma of superficial urothelial cells indicates a role for these components in passively maintaining the blood-urine barrier. The observed distribution of Na+,K+-ATPase in mid and deep urothelial cells implicates this enzyme and these cells in actively maintaining the urine's hypertonicity. Basal urothelial cells contained glycoconjugate with terminal galactose in their plasmalemma. Ultrastructural features suggesting involution of superficial urothelial cells further evidence restriction of active ion transport to the deeper cells.
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PMID:Evidence for the blood-urine barrier depending on urothelium and carbonic anhydrase positive fibroblasts. 244 48

To test the possibility that ATP diffusion limits the kinetics of myosin ATPase (EC. 3.6.1.3) in situ, myosin was covalently bound to the surface of 2 kinds of films: collagen and Immunodyne. On collagen films, it was bound either with 1-ethyl-3 (3 dimethyl-aminopropyl)carbodiimide (EDC) or with dimethyl-3,3'-dithiobis(propionimidate) (DTP). The apparent Km for K+-ATP rose from 0.26 mM for free myosin in solution to 2-5 mM for covalently bound myosin, and maximum K+-ATPase activity was very low. With the other film, Immunodyne from Pall, the maximum activity of bound myosin was 170 nmol per min per 1.5 cm2 film. The apparent Km for K+-ATP was 2.1 mM when the incubation mixture was vigorously stirred, and the effect of stirring indicated that the kinetics of K+-ATP hydrolysis are limited by external diffusion. The large amount of myosin bound per unit of Immunodyne film surface permitted the study of Mg2+-ATPase activity, although it was 400-500 times less than the K+-ATPase activity. The apparently non-Michaelian kinetics of Mg2+-ATP hydrolysis are attributable to the external diffusion. The apparent Michaelis constant observed at low Mg2+-ATP concentrations rose from 0.27 microM for myosin in solution to 5 microM for myosin bound to Immunodyne film.
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PMID:Diffusion-limited kinetics of immobilized myosin ATPase. 252 82

The myosin isozyme distribution in the left ventricle and in the interventricular septum of rabbits was studied after 3, 7, 11, 14 and 21 days of L-thyroxine (500 micrograms/kg/day) administration. Histochemical procedures were employed to identify V1 and V3 by their Ca2+ ATPase activity and their proportions were quantified through polyacrylamide gel electrophoresis. In the left ventricle, the subepicardium was the first to show the shift from V3 to V1, followed by the subendocardium. The intermediate region became heterogeneous by 11 days and remained so until 21 days. The right subendocardial and the intermediate regions of the interventricular septum were heterogeneous in the normal rabbit and hyperthyroidism resulted in a shift from V3 to V1 in both the right and left subendocardial regions of the septum. Like the left ventricle, the intermediate region of the interventricular septum remained heterogeneous. Localized accumulations of collagen were seen in all regions of the left ventricle and interventricular septum. From these results we conclude that in thyrotoxic myocardial hypertrophy the isozymic shift from V3 to V1 is progressive, region-specific and is directly correlated with the period of hyperthyroidism in the first 2 weeks. Prolonged hyperthyroidism results in localized accumulation of collagen which does not exhibit any regional specificity.
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PMID:Changes in myosin isozyme expression during cardiac hypertrophy in hyperthyroid rabbits. 252 81


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