Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

Resolution of pulmonary edema involved active transepithelial sodium transport. Although several of the cellular and molecular mechanisms involved are relatively well understood, it is only recently that the regulation of these mechanisms in injured lung are being evaluated. Interestingly, in mild-to-moderate lung injury, alveolar edema fluid clearance is often preserved. This preserved or enhanced alveolar fluid clearance is mediated by catecholamine-dependent or -independent mechanisms. This stimulation of alveolar liquid clearance is related to activation or increased expression of sodium transport molecules such as the epithelial sodium channel or the Na(+)-K(+)-ATPase pump and may also involve the cystic fibrosis transmembrane conductance regulator. When severe lung injury occurs, the decrease in alveolar liquid clearance may be related to changes in alveolar permeability or to changes in activity or expression of sodium or chloride transport molecules. Multiple pharmacological tools such as beta-adrenergic agonists, vasoactive drugs, or gene therapy may prove effective in stimulating the resolution of alveolar edema in the injured lung.
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PMID:Lung edema clearance: 20 years of progress: invited review: alveolar edema fluid clearance in the injured lung. 1243 40

Pyrethroids are used widely as insecticides both in agriculture and in households. A cellular target of pyrethroids is the sodium channel in the membrane. In the present study, the activity of the membrane bound integral protein ATPase was studied as a biomarker for the membrane effect of the pyrethroids permethrin and cypermethrin. Male Sprague-Dawley rats were used for cerebral synaptosome preparation. The isolation of synaptosomes was performed with the Percoll gradient method. Both total ATPase and Mg(2+) activated ATPase were studied by determining inorganic phosphate liberated from the substrate ATP. One hour exposure to permethrin (Biokill) and cypermethrin (Ripcord) insecticide products affected ATPase activities. The activity of Na(+), K(+) ATPase decreased dose-dependently in 10-50 microM concentrations of permethrin, and Mg(2+) activated ATPase increased over twofold in the same concentrations of the active components. The effect of the cypermethrin compound Ripcord was not clearly dose-dependent. The activity of total ATPase was almost entirely lost in the concentrations of 100 microM of permethrin and cypermethrin. The results support the idea that membrane ATPases are one target of the neurotoxic effect of pyrethroid compounds.
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PMID:The synaptosomal membrane bound ATPase as a target for the neurotoxic effects of pyrethroids, permethrin and cypermethrin. 1261 99

Interactions between chondrocytes and their extracellular matrix are partly mediated by beta1-integrin receptors. Recent studies have shown that beta1-integrins co-localize with a variety of cytoskeletal complexes, signaling proteins and growth factor receptors. Since mechanosensitive ion channels and integrins have been proposed to participate in skeletal mechanotransduction, in this study, we investigated the possible co-localization of beta1-integrins with two ion channels and a P-type ATPase in mouse limb-bud chondrocytes. The alpha subunits of Na, K-ATPase, the epithelial sodium channel (ENaC) and the voltage activated calcium channel (VACC) were immunostained in organoid cultures derived from limb-buds of 12-day-old mice using well-characterized antibodies. Indirect immunofluorescence revealed abundant expression of beta1-integrins and each of the selected systems in limb-bud chondrocytes. Two-fluorochrome immunostaining demonstrated that beta1-integrin, Na, K-ATPase, ENaC and VACC co-localize in chondrocytes. Co-imunoprecipitation experiments revealed co-localization and association of integrins with ENaC, VACC and Na, K-ATPase. Cellular responses and signaling cascades initiated by the influx of calcium or sodium through putative mechanosensitive channels may be regulated more effectively if such channels were organized around integrins with receptors, kinases and cytoskeletal complexes clustered about them. The close proximity of ATPase ion pumps such as Na, K-ATPase to chondrocyte mechanoreceptor complexes could facilitate rapid homeostatic responses to the ionic perturbations brought about by activation of mechanically gated cation channels and efficiently regulate the intracellular milieu of chondrocytes.
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PMID:Beta1-integrins co-localize with Na, K-ATPase, epithelial sodium channels (ENaC) and voltage activated calcium channels (VACC) in mechanoreceptor complexes of mouse limb-bud chondrocytes. 1264 83

Sodium-water balance is causally linked to the functional expression of a number of important ocular tissues, viz. corneal deturgescence, aqueous humor secretion by the iris, hydration of the lens, retinal photoreception, and choriocapillary angiogenesis. The regulation of sodium absorption in the eye is generally believed to be under the control of Na(+),K(+)-activated adenosine triphosphatase, although evidence for this view is at best circumstantial. Contemporary work has shown widespread distribution of the mineralocorticoid hormone receptor and its colocalization with the amiloride-sensitive sodium channel in cells of diverse embryological origins. All available evidence favors the idea that the transcriptional regulation of the apical sodium channel by adrenocorticoids, and not the basolateral sodium pump, is critically important to sodium-water homeostasis in various ocular tissues, in a manner previously believed to be limited exclusively to the epithelial cell in various peripheral organs. Based upon these parameters, models are presented to help in understanding the direction of sodium absorption in a number of ocular tissues. Thus, the regulation of the sodium channel by steroid hormones seems to be a universal feature of the living cell that may have important implications in the understanding and management of normal ocular functions and their modification in human pathology.
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PMID:Receptor-mediated adrenocorticoid hormone signaling in ocular tissues. 1269 62

Transforming growth factor-beta1 (TGF-beta 1) may be a critical mediator of lung injury and subsequent remodeling during recovery. We evaluated the effects of TGF-beta 1 on the permeability and active ion transport properties of alveolar epithelial cell monolayers. Rat alveolar type II cells plated on polycarbonate filters in defined serum-free medium form confluent monolayers and acquire the phenotypic characteristics of alveolar type I cells. Exposure to TGF-beta 1 (0.1-100 pM) from day 0 resulted in a concentration- and time-dependent decrease in transepithelial resistance (Rt) and increase in short-circuit current (Isc). Apical amiloride or basolateral ouabain on day 6 inhibited Isc by 80 and 100%, respectively. Concurrent increases in expression of Na+-K+-ATPase alpha 1- and beta 1-subunits were observed in TGF-beta 1-treated monolayers. No change in the alpha-subunit of the rat epithelial sodium channel (alpha-rENaC) was seen. Exposure of confluent monolayers to TGF-beta 1 from day 4 resulted in an initial decrease in Rt within 6 h, followed by an increase in Isc over 72-96 h. These results demonstrate that TGF-beta 1 modulates ion conductance and active transport characteristics of the alveolar epithelium, associated with increased Na+-K+-ATPase, but without a change in alpha-rENaC.
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PMID:Modulation of ion conductance and active transport by TGF-beta 1 in alveolar epithelial cell monolayers. 1460 49

To determine the impact of transplantation-associated injury on the clearance mechanisms of pulmonary edema, we created a canine single lung transplant model. After 3 hours of preservation and 4 hours of reperfusion, right native lungs and left transplanted lungs were used to measure alveolar liquid clearance (ALC) in ex vivo liquid-filled lung preparations. We also examined the role of the pulmonary circulation in edema clearance in in vivo liquid-filled lungs between 4 and 8 hours of reperfusion. To study molecular modifications in ALC, we also measured expression levels of the epithelial sodium channel (ENaC) and sodium-potassium-adenosine triphosphatase (ATPase). We found that ALC was significantly lower in transplanted than in right native lungs ex vivo (p < 0.05) and that transplanted lungs did not respond to the beta-adrenergic agonist terbutaline. Our in vivo study confirmed the ex vivo results. Molecular analyses revealed that ENaC messenger RNA but not sodium-potassium-ATPase was significantly decreased in transplanted lungs (p < 0.01). Furthermore, there was a significant decrease in ENaC protein expression. Therefore, we conclude that the current investigation indicates that the lung injury caused by lung preservation and transplantation significantly reduces the edema clearance ability of transplanted lungs.
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PMID:Alveolar liquid clearance and sodium channel expression are decreased in transplanted canine lungs. 1273 1

In several in vivo settings, prolonged alterations in the rate of apical Na+ entry into epithelial cells alter the ability of these cells to reabsorb Na+. We previously modeled this load dependence of transport in A6 cells by either decreasing Na+ entry via apical Na+ removal or amiloride or enhancing Na+ entry by chronic short-circuiting (Rokaw MD, Sarac E, Lechman E, West M, Angeski J, Johnson JP, and Zeidel ML. Am J Physiol Cell Physiol 270: C600-C607, 1996). Inhibition of Na+ entry by either method was associated with striking downregulation of transport rate as measured by short-circuit current (Isc), which recovered to basal levels of transport over a period of hours. Conversely, upregulation of Na+ entry by short-circuiting resulted in a sustained increase in transport rate that also returned to basal levels over a period of hours. The current studies were undertaken to determine whether these conditions were associated with alterations in either the whole cell content or apical membrane distribution of sodium channel (ENaC) subunits or on basolateral expression of either of the subunits of the Na+-K+-ATPase. We compared these effects to those achieved by chronic upregulation of Na+ transport by aldosterone. Whole cell levels of ENaC subunits were measured by immunoblot following 18-h inhibition of Na+ entry achieved by either tetramethylammonium replacement of Na+ or apical amiloride or after an 18-h increase in Na+ entry achieved by chronic short-circuiting. None of these maneuvers significantly altered the whole cell content of any of the ENaC subunits compared with control cells. We then examined the effects of these maneuvers on apical membrane ENaC expression using domain-specific biotinylation and immunoblot. Inhibition of Na+ entry by either method was associated with a profound decrease in apical membrane beta-ENaC without significant changes in apical membrane alpha-or gamma-ENaC amounts. Restoration of apical Na+ and/or removal of amiloride resulted in return of Isc to control levels over 2 h and coincided with return of apical beta-ENaC to control levels without change in apical alpha- or gamma-ENaC. Stimulation of Na+ transport by short-circuiting, in contrast, did not significantly alter apical membrane composition of any of the ENaC subunits. Basolateral expression of Na+-K+-ATPase was also measured by biotinylation and immunoblot and was unchanged under all conditions. Aldosterone increased basolateral expression of the alpha-subunit of Na+-K+-ATPase. These results suggest that chronic downregulation of transport is mediated, in part, by a selective decrease in apical membrane ENaC expression, consistent with our previous observations of noncoordinate regulation of ENaC expression under varying transport conditions in A6 cells. The chronic increase in the rate of Na+ entry is not associated with any of the changes in transporter density at either apical or basolateral membrane seen with aldosterone, suggesting that these two mechanisms of augmenting transport are completely distinct.
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PMID:Effect of altered Na+ entry on expression of apical and basolateral transport proteins in A6 epithelia. 1274 57

Cochlear sensory transduction depends on active extrusion of sodium ion (Na(+)) from the luminal fluid, endolymph. Reissner's membrane epithelium forms much of the barrier between cochlear endolymph and perilymph and we hypothesized that Reissner's membrane might be responsible for this function. We found that Reissner's membrane isolated from gerbil produced a short circuit current (I(sc)) directed into the apical side, consistent with cation absorption and/or anion secretion. I(sc) was inhibited by amiloride analogs in the potency sequence benzamil>amiloride>>ethylisopropylamiloride, consistent with Na(+) absorption through an epithelial sodium channel in the apical cell membrane. I(sc) was also inhibited by an inhibitor of Na(+),K(+)-ATPase, ouabain, and by the K(+) channel blockers Ba(2+), 4-aminopyridine and quinine but not tetraethylammonium nor glibenclamide, consistent with the presence of a voltage-activated K(+) channel. Bumetanide, an inhibitor of the Na(+),2Cl(-),K(+)-cotransporter, had no effect on I(sc). Contrary to previous hypotheses, no evidence was found for electrogenic secretion of Cl(-) under control of cAMP since neither forskolin nor genistein affected I(sc) when Na(+) absorption was blocked. These results provide the first direct evidence that Reissner's membrane contributes to normal cochlear function by absorption of Na(+) from endolymph.
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PMID:Endolymphatic sodium homeostasis by Reissner's membrane. 1276 62

In mineralocorticoid target tissues, 11beta-hydroxysteroid dehydrogenase type 2 (11beta-HSD2) confers mineralocorticoid receptor selectivity by metabolizing hormonally active cortisol to inactive cortisone, allowing aldosterone access to the receptor. This enzyme is also expressed in high abundance in fetal tissues, particularly in placental trophoblast, where a role has been proposed in regulating fetal growth and development by protecting the fetus from maternal hypercortisolaemia and modulating local glucocorticoid receptor (GR), rather than mineralocorticoid receptor-mediated responses. As such the placenta has not been considered a mineralocorticoid target tissue. We have used conventional RT-PCR and real-time quantitative RT-PCR to demonstrate that primary cultures of term human cytotrophoblast express the mineralocorticoid-responsive genes Na/K-ATPase (alpha1 and beta1 subunits), epithelial sodium channel (ENaC, alpha and gamma subunits) and the serum and glucocorticoid-inducible kinase (SGK). SGK expression was found to be rapidly and strongly induced by corticosteroids (24- and 38-fold by 10(-7) mol/l aldosterone and 10(-7) mol/l dexamethasone respectively after 1 h). Dexamethasone-, but not aldosterone-stimulated SGK induction was inhibited by GR antagonist (RU38486), confirming the presence of a functional mineralocorticoid receptor and suggesting that placental trophoblast expresses a functional mineralocorticoid receptor, which is in part responsible for the corticosteroid regulation of SGK expression. Placental 11beta-HSD2 may protect the MR in a fashion analogous to classical mineralocorticoid tissues to modulate trophoblast sodium transport.
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PMID:Characterization of human trophoblast as a mineralocorticoid target tissue. 1461 41

Current understanding of chloride cells (CCs) is briefly reviewed with emphasis on molecular aspects of their channels, transporters and regulators. Seawater-type and freshwater-type CCs have been identified based on their shape, location and response to different ionic conditions. Among the freshwater-type CCs, subpopulations are emerging that are implicated in the uptake of Na(+), Cl(-) and Ca(2+), respectively, and can be distinguished by their shape of apical crypt and affinity for lectins. The major function of the seawater CC is transcellular secretion of Cl(-), which is accomplished by four major channels and transporters: (1). CFTR Cl(-) channel, (2). Na(+),K(+)-ATPase, (3). Na(+)/K(+)/2Cl(-) cotransporter and (4). a K(+) channel. The first three components have been cloned and characterized, but concerning the K(+) channel that is essential for the continued generation of the driving force by Na(+),K(+)-ATPase, only one candidate is identified. Although controversial, freshwater CCs seem to perform the uptake of Na(+), Cl(-) and Ca(2+) in a manner analogous to but slightly different from that seen in the absorptive epithelia of mammalian kidney and intestine since freshwater CCs face larger concentration gradients than ordinary epithelial cells. The components involved in these processes are beginning to be cloned, but their CC localization remains to be established definitively. The most important yet controversial issue is the mechanism of Na(+) uptake. Two models have been postulated: (i). the original one involves amiloride-sensitive electroneutral Na(+)/H(+) exchanger (NHE) with the driving force generated by Na(+),K(+)-ATPase and carbonic anhydrase (CA) and (ii). the current model suggests that Na(+) uptake occurs through an amiloride-sensitive epithelial sodium channel (ENaC) electrogenically coupled to H(+)-ATPase. While fish ENaC remains to be identified by molecular cloning and database mining, fish NHE has been cloned and shown to be highly expressed on the apical membrane of CCs, reviving the original model. The CC is also involved in acid-base regulation. Analysis using Osorezan dace (Tribolodon hakonensis) living in a pH 3.5 lake demonstrated marked inductions of Na(+),K(+)-ATPase, CA-II, NHE3, Na(+)/HCO(3)(-) cotransporter-1 and aquaporin-3 in the CCs on acidification, leading to a working hypothesis for the mechanism of Na(+) retention and acid-base regulation.
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PMID:Molecular biology of major components of chloride cells. 1466 88


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