Ouabain‐sensitive H,K‐ATPase: tissue‐specific expression of the mammalian genes encoding the catalytic α subunit<sup>1</sup>

Pestov, Nikolay B.; Romanova, L. G.; Korneenko, Tatyana V.; Egorov, Maxim; Костина, М. Б.; Sverdlov, Vladimir E.; Askari, Amir; Shakhparonov, M. I.; Modyanov, Nikolaï N.

doi:10.1016/s0014-5793(98)01483-5

Cited by 43 publications

(42 citation statements)

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“…The underlying mechanism remains unexplained. It has been revealed that both gastric and non-gastric type of hydrogen/potassium adenosine triphosphatase (H+/ K+-exchanging ATPase) is present in various tissues including cochlear lateral wall, polymorphonuclear leukocytes, kidney, brain, placenta and colon but its functional role has not been well studied (14,23,24).…”

Section: Discussionmentioning

confidence: 99%

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

2017

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Ključne besede:gastroezofagealna refluksna bolezen; otrok; inhibitorji protonske črpalke; H2-blokatorji; eozinofilni ezofagitis; na inhibitor protonske črpalke odzivna ezofagealna eozinofilija Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report Klinični primer razvoja urinske inkontinence pri 7-letnem fantu med zdravljenjem z inhibitorjem protonske črpalke in izginotje kliničnopatoloških znakov eozinofilnega ezofagitisa po zdravljenju z antagonisti H2 receptorjev AbstractBackground: Several diseases result in profound infiltration of esophageal mucosa by eosinophilic granulocites, with gastroesophageal reflux disease (GERD), eosinophilic esophagitis (EoE) and proton-pump-inhibitor-responsive esophageal eosinophilia (PPI-REE) being the most prevalent. Proton-pump-inhibitor-responsive esophageal eosinophilia (PPI-REE) is a newly recognized entity that must be differentiated from eosinophilic esophagitis (EoE).Case presentation: A 7-year old Slovenian male presented with a few-month history of chest pain, regurgitation and heartburn. First endoscopy was performed and revealed pronounced longitudinal furrows, and on hystology examination > 70 eosinophils per high power field were found through the entire thickness of epithelium and in the submucosis with eosinophilic microabscess formation. Results of 24-hour pH-monitoring (without impedance monitoring) excluded pathologic acid reflux. All allergy tests were negative. The patient started treatment with proton pump inhibitors (PPIs) for three times, twice with pantoprazole before the endoscopy and once with esomeprasole after it to exclude the diagnosis of GERD and PPI-REE. Urinary incontinence reappeared each time just few days after starting treatment and disapeared few days after stopping it. Therefore, urinary incontinence was considered as a plausible adverse effect of therapy with PPIs. As treatment with PPIs was not tolerated, a therapy with H2-receptor antagonists ranitidine was applied for more than 2 months followed by a second endoscopy. Both symptoms and esophageal eosinophilia completely resolved with ranitidine. The resolution of esophageal eosinophilia in PPI-REE has been atributed to proton pump independent antiinflammatory effects of PPIs. No such effects have been described in H2-receptor antagonists. Conclusions:Two unique phenomena were observed in the pediatric patient with profound esophageal eosinophilia: urinary incontinence as an adverse effect of therapy with PPIs, and complete resolution of esophageal eosinophilic inflammation with typical features of EoE after treatment with H2-receptor antagonists. IzvlečekIzhodišča: Mnoge bolezni lahko privedejo do obsežne infiltracije sluznice požiralnika z eozinofilnimi granulociti. Med njimi so najbolj pogoste gastroezofagealna refluksna bolezen, eozinofilni ezofagitis in na inhibitor protonske črpalke odzivna ezofag...

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Section: Discussionmentioning

confidence: 99%

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

2017

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“…Given ouabain was used as a specific blocker for Na + -K + -ATPase in these studies, and the location of Na + -K + -ATPase has not been verified immunocytochemically, we should keep in mind that ouabain-inhibitable H + -K + -ATPase α subunit may co-exist [35,36]. H + -K + -ATPase has been found in re-absorptive epithelial tissues, including kidney and gastrointestinal tract [36,37].…”

Section: I-2 Na + -K + -Atpase and Ca 2+ -Atpasementioning

confidence: 99%

Electrolyte and Fluid Transport in Mesothelial Cells

Ji¹,

Nie²

2008

JEBP

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Mesothelial cells are specialized epithelial cells, which line the pleural, pericardial, and peritoneal cavities. Accumulating evidence suggests that the monolayer of mesothelial cells is permeable to electrolyte and fluid, and thereby govern both fluid secretion and re-absorption in the serosal cavities. Disorders in these salt and fluid transport systems may be fundamental in the pathogenesis of pleural effusion, pericardial effusion, and ascites. In this review, we discuss the location, physiological function, and regulation of active transport (Na + -K + -ATPase) systems, cation and anion channels (Na + , K + , Cl − , and Ca 2+ channels), antiport (exchangers) systems, and symport (co-transporters) systems, and water channels (aquaporins). These secretive and absorptive pathways across mesothelial monolayer cells for electrolytes and fluid may provide pivotal therapeutical targets for novel clinical intervention in edematous diseases of serous cavities. Keywords mesothelioma; ion channel; permeability; effusion; filtration; ENaC Mesothelial cells are specialized epithelial cells that line the serous cavities, including the pleural, pericardial, and peritoneal cavities in addition to internal organs [1]. While the mesothelium was first described more than a century ago, one of its critical essential functions, namely, its active roles in transerosal transport, in particular, cavity fluid secretion and reabsorption, was long overlooked. Only in last two decades compelling evidence accumulated that mesothelial cells actively transport electrolytes and fluid and, in turn, regulate liquid volume within the cavities. The mesothelium, on the basis of recent increasing experimental evidence, both in vitro and in vivo, is less permeable to electrolytes than was previously assumed, with ion permeability characteristics similar to those in epithelia [2,3]. Herein this article we will review the expression and biophysical features of salt and fluid transport systems, both active and passive, that have been identified in mesothelial cells (Fig. 1, Tables 1 and 2). I. ION CHANNELS AND ATPASE I-1. Amiloride-Inhibitable Cation ChannelsThe epithelial sodium channel (ENaC), as a major pathway which participates in sodium movement across the apical membrane of polarized epithelial cells, has been cloned and characterized [4][5][6] ENaC subunits have been cloned to date, namely α-, β-, γ-, δ-, and ε-ENaC [7]. The biophysical properties of various ENaC channels depend on their subunit compositions. When expressed in oocytes one of "conductive" subunits (α, δ, and ε-ENaC) can form a channel sharing identical biophysical properties to three-subunit channels composed of both a "conductive" subunit and two "non-conductive" subunits, namely, β-and γ-ENaCs. When α-, β-, and γ-ENaC subunits are assembled together, the result is a 4-to 6-pS channel that is highly selective for Na + over K + . In contrast, two-subunit α β-and α γ-ENaC channels display diverse amiloride sensitivity, conductance, and Na + permeability [8]. ENaC is...

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“…The fact that transgene expression was detected at low levels in the brain and lung by immunoblot analysis of EGFP expression indicates that the mechanism for silencing of the HK␣ 2 gene in the distal colon may be specific to that tissue. Furthermore, the finding of HK␣ 2 transgene expression in the brain and lung was not surprising, because HK␣2 mRNA expression has been reported in the brain from the mouse and rabbit, and the homologous ATP1AL1 mRNA has been detected in the human brain (21). A role of HK␣ 2 in the brain or lung function has not been established.…”

Section: Discussionmentioning

confidence: 99%

In vivo expression profile of a H⁺-K⁺-ATPase α₂-subunit promoter-reporter transgene

Zhang¹,

Xia²,

Zou³

et al. 2004

American Journal of Physiology-Renal Physiology

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Because little is known about the molecular basis of transcriptional regulation of the murine H+-K+-ATPase α2 (HKα2) gene or other genes whose expression is restricted in part to the collecting duct, especially in vivo, we developed transgenic mice carrying an insertional HKα2 promoter-reporter gene construct. In these mice, the region −7,264/+253 of the HKα2 5′-flanking region controls expression of the reporter gene enhanced green fluorescent protein (EGFP). Patterns of HKα2/EGFP transgene expression were examined by fluorescence microscopy and immunoblotting. Of 10 major organs examined, EGFP immunoreactivity was detected abundantly in the kidney, and to a far lesser extent, in the brain and lung. Within the kidney, EGFP fluorescence was detected exclusively in the collecting ducts of transgenic mice and colocalized with the cellular distribution of both endogenous HKα2 and aquaporin-2, consistent with the known expression pattern of endogenous HKα2 in principal cells. Surprisingly, no transgene expression was evident by immunoblotting or fluorescence microscopy in the distal colon, the site of the highest endogenous HKα2 expression. Although previous studies of steady-state mRNA levels suggested differences in HKα2 gene regulation in the kidney and colon, our results provide the first direct evidence of differential transcriptional control of the HKα2 gene in these organs and suggest that regions outside the 5′-flanking region or other regulatory factors play a role in HKα2 expression in the distal colon.

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Ouabain‐sensitive H,K‐ATPase: tissue‐specific expression of the mammalian genes encoding the catalytic α subunit¹

Abstract: Human ATP1AL1 and corresponding genes of other mammals encode the catalytic K

Cited by 43 publications

References 25 publications

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

Electrolyte and Fluid Transport in Mesothelial Cells

In vivo expression profile of a H⁺-K⁺-ATPase α₂-subunit promoter-reporter transgene

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Ouabain‐sensitive H,K‐ATPase: tissue‐specific expression of the mammalian genes encoding the catalytic α subunit1

Abstract: Human ATP1AL1 and corresponding genes of other mammals encode the catalytic K

Cited by 43 publications

References 25 publications

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

Development of urinary incontinence in a 7-year old boy after therapy with proton pump inhibitors and complete resolution of his clinicopathologic features of eosinophilic esophagitis after H2-receptor antagonist treatment: A case report

Electrolyte and Fluid Transport in Mesothelial Cells

In vivo expression profile of a H+-K+-ATPase α2-subunit promoter-reporter transgene

Contact Info

Product

Resources

About

Ouabain‐sensitive H,K‐ATPase: tissue‐specific expression of the mammalian genes encoding the catalytic α subunit¹

In vivo expression profile of a H⁺-K⁺-ATPase α₂-subunit promoter-reporter transgene