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  4. Monthly Traffic Estimate
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We are analyzing https://link.springer.com/article/10.1007/s00424-013-1342-9.

Title:
Ion transporters in brain endothelial cells that contribute to formation of brain interstitial fluid | PflĂźgers Archiv - European Journal of Physiology
Description:
Ions and water transported across the endothelium lining the blood–brain barrier contribute to the fluid secreted into the brain and are important in maintaining appropriate volume and ionic composition of brain interstitial fluid. Changes in this secretion process may occur after stroke. The present study identifies at transcript and protein level ion transporters involved in the movement of key ions and examines how levels of certain of these alter following oxidative stress. Immunohistochemistry provides evidence for Cl−/HCO3 − exchanger, AE2, and Na+, HCO3 − cotransporters, NBCe1 and NBCn1, on brain microvessels. mRNA analysis by RT-PCR reveals expression of these transporters in cultured rat brain microvascular endothelial cells (both primary and immortalized GPNT cells) and also Na+/H+ exchangers, NHE1 (primary and immortalized) and NHE2 (primary cells only). Knock-down using siRNA in immortalized GPNT cells identifies AE2 as responsible for much of the Cl−/HCO3 − exchange following extracellular chloride removal and NHE1 as the transporter that accounts for most of the Na+/H+ exchange following intracellular acidification. Transcript levels of both AE2 and NHE1 are increased following hypoxia/reoxygenation. Further work is now required to determine the localization of the bicarbonate transporters to luminal or abluminal membranes of the endothelial cells as well as to identify and localize additional transport mechanisms that must exist for K+ and Cl−.
Website Age:
28 years and 1 months (reg. 1997-05-29).

Matching Content Categories {📚}

  • Science
  • Education
  • Health & Fitness

Content Management System {📝}

What CMS is link.springer.com built with?

Custom-built

No common CMS systems were detected on Link.springer.com, and no known web development framework was identified.

Traffic Estimate {📈}

What is the average monthly size of link.springer.com audience?

🌠 Phenomenal Traffic: 5M - 10M visitors per month


Based on our best estimate, this website will receive around 5,000,019 visitors per month in the current month.
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How Does Link.springer.com Make Money? {💸}

We're unsure if the website is profiting.

While many websites aim to make money, others are created to share knowledge or showcase creativity. People build websites for various reasons. This could be one of them. Link.springer.com could be getting rich in stealth mode, or the way it's monetizing isn't detectable.

Keywords {🔍}

cells, brain, nhe, google, scholar, cas, pubmed, article, rat, endothelial, transporters, bloodbrain, shown, barrier, hco, exchange, gpnt, transport, blood, fluid, fig, cell, sections, expression, ion, secretion, nah, physiol, nbce, microvessels, mrna, sirna, csf, medium, interstitial, clhco, nbcn, net, activity, antibody, luminal, isf, membrane, antibodies, channels, evidence, phi, data, cultured, rate,

Topics {✒️}

goat anti-mouse igg ion-selective micro-electrode method article download pdf brain microvascular endothelial-cells—properties osmotherapy-mediated rebound response n-ethyl-n-isopropyl sanofi-aventis deutschland gmbh high-resolution immunogold cytochemistry von weikersthal sf wax-embedded rat brain blood–retinal barriers retain brain capillary endothelial-cells compromised blood–brain barrier blood–brain barrier transport high-resolution optical images astroglial cell-induced expression electrogenic na/hco2 cotransporter dids-sensitive slc4a transporters constitutively water-permeable segments twenty-micrometre sections cut blood–brain-barrier permeability blood–brain barrier secretion blood–brain barrier na/ blood–brain barrier na blood–cerebrospinal fluid barriers nominally bicarbonate-free medium rat caudate-nucleus background-corrected emissions measured cross cell membranes rt-pcr reveals expression rheogenic sodium-bicarbonate cotransport blood–brain barrier contribute european economic area ph-sensitive wavelength 502 nm ion transport/fluid secretion external hepes-buffered solution ph-insensitive wavelength 440 nm endothelial cells derived volume-sensitive chloride current reporter gene construct weak base trapping privacy choices/manage cookies ischemic cerebral edema related subjects null mice exhibit cerebral interstitial fluid wax-embedded tissue volume-activated cl− channel focal cerebral ischemia schielke gp

Schema {🗺️}

WebPage:
      mainEntity:
         headline:Ion transporters in brain endothelial cells that contribute to formation of brain interstitial fluid
         description:Ions and water transported across the endothelium lining the blood–brain barrier contribute to the fluid secreted into the brain and are important in maintaining appropriate volume and ionic composition of brain interstitial fluid. Changes in this secretion process may occur after stroke. The present study identifies at transcript and protein level ion transporters involved in the movement of key ions and examines how levels of certain of these alter following oxidative stress. Immunohistochemistry provides evidence for Cl−/HCO3 − exchanger, AE2, and Na+, HCO3 − cotransporters, NBCe1 and NBCn1, on brain microvessels. mRNA analysis by RT-PCR reveals expression of these transporters in cultured rat brain microvascular endothelial cells (both primary and immortalized GPNT cells) and also Na+/H+ exchangers, NHE1 (primary and immortalized) and NHE2 (primary cells only). Knock-down using siRNA in immortalized GPNT cells identifies AE2 as responsible for much of the Cl−/HCO3 − exchange following extracellular chloride removal and NHE1 as the transporter that accounts for most of the Na+/H+ exchange following intracellular acidification. Transcript levels of both AE2 and NHE1 are increased following hypoxia/reoxygenation. Further work is now required to determine the localization of the bicarbonate transporters to luminal or abluminal membranes of the endothelial cells as well as to identify and localize additional transport mechanisms that must exist for K+ and Cl−.
         datePublished:2013-09-11T00:00:00Z
         dateModified:2013-09-11T00:00:00Z
         pageStart:887
         pageEnd:901
         sameAs:https://doi.org/10.1007/s00424-013-1342-9
         keywords:
            Rat brain endothelial cells
            Blood–brain barrier
            Brain interstitial fluid
            Cl−/HCO3 − exchanger AE2
            Na+, HCO3 − cotransporters, NBCe1 and NBCn1
            Na+/H+ exchangers NHE1 and NHE2
            Human Physiology
            Molecular Medicine
            Neurosciences
            Cell Biology
            Receptors
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            name:PflĂźgers Archiv - European Journal of Physiology
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                        name:Department of Pharmacology, University of Cambridge, Cambridge, UK
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               name:Stephen B. Hladky
               affiliation:
                     name:University of Cambridge
                     address:
                        name:Department of Pharmacology, University of Cambridge, Cambridge, UK
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                     type:Organization
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ScholarlyArticle:
      headline:Ion transporters in brain endothelial cells that contribute to formation of brain interstitial fluid
      description:Ions and water transported across the endothelium lining the blood–brain barrier contribute to the fluid secreted into the brain and are important in maintaining appropriate volume and ionic composition of brain interstitial fluid. Changes in this secretion process may occur after stroke. The present study identifies at transcript and protein level ion transporters involved in the movement of key ions and examines how levels of certain of these alter following oxidative stress. Immunohistochemistry provides evidence for Cl−/HCO3 − exchanger, AE2, and Na+, HCO3 − cotransporters, NBCe1 and NBCn1, on brain microvessels. mRNA analysis by RT-PCR reveals expression of these transporters in cultured rat brain microvascular endothelial cells (both primary and immortalized GPNT cells) and also Na+/H+ exchangers, NHE1 (primary and immortalized) and NHE2 (primary cells only). Knock-down using siRNA in immortalized GPNT cells identifies AE2 as responsible for much of the Cl−/HCO3 − exchange following extracellular chloride removal and NHE1 as the transporter that accounts for most of the Na+/H+ exchange following intracellular acidification. Transcript levels of both AE2 and NHE1 are increased following hypoxia/reoxygenation. Further work is now required to determine the localization of the bicarbonate transporters to luminal or abluminal membranes of the endothelial cells as well as to identify and localize additional transport mechanisms that must exist for K+ and Cl−.
      datePublished:2013-09-11T00:00:00Z
      dateModified:2013-09-11T00:00:00Z
      pageStart:887
      pageEnd:901
      sameAs:https://doi.org/10.1007/s00424-013-1342-9
      keywords:
         Rat brain endothelial cells
         Blood–brain barrier
         Brain interstitial fluid
         Cl−/HCO3 − exchanger AE2
         Na+, HCO3 − cotransporters, NBCe1 and NBCn1
         Na+/H+ exchangers NHE1 and NHE2
         Human Physiology
         Molecular Medicine
         Neurosciences
         Cell Biology
         Receptors
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                     type:PostalAddress
                  type:Organization
            type:Person
            name:Shanshan Wang
            affiliation:
                  name:University of Cambridge
                  address:
                     name:Department of Pharmacology, University of Cambridge, Cambridge, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Caroline J. Taylor
            affiliation:
                  name:University of Melbourne, St. Vincent’s Hospital
                  address:
                     name:O’Brien Institute and Department of Surgery, University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia
                     type:PostalAddress
                  type:Organization
                  name:Australian Catholic University
                  address:
                     name:Faculty of Health Sciences, Australian Catholic University, Melbourne, Australia
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Margery A. Barrand
            affiliation:
                  name:University of Cambridge
                  address:
                     name:Department of Pharmacology, University of Cambridge, Cambridge, UK
                     type:PostalAddress
                  type:Organization
            type:Person
            name:Stephen B. Hladky
            affiliation:
                  name:University of Cambridge
                  address:
                     name:Department of Pharmacology, University of Cambridge, Cambridge, UK
                     type:PostalAddress
                  type:Organization
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            type:Person
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         type:PostalAddress
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      address:
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         type:PostalAddress
      name:Australian Catholic University
      address:
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         type:PostalAddress
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      address:
         name:Department of Pharmacology, University of Cambridge, Cambridge, UK
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         type:PostalAddress
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Person:
      name:Ruth Mokgokong
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Pharmacology, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Shanshan Wang
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Pharmacology, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Caroline J. Taylor
      affiliation:
            name:University of Melbourne, St. Vincent’s Hospital
            address:
               name:O’Brien Institute and Department of Surgery, University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia
               type:PostalAddress
            type:Organization
            name:Australian Catholic University
            address:
               name:Faculty of Health Sciences, Australian Catholic University, Melbourne, Australia
               type:PostalAddress
            type:Organization
      name:Margery A. Barrand
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Pharmacology, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      name:Stephen B. Hladky
      affiliation:
            name:University of Cambridge
            address:
               name:Department of Pharmacology, University of Cambridge, Cambridge, UK
               type:PostalAddress
            type:Organization
      email:[email protected]
PostalAddress:
      name:Department of Pharmacology, University of Cambridge, Cambridge, UK
      name:Department of Pharmacology, University of Cambridge, Cambridge, UK
      name:O’Brien Institute and Department of Surgery, University of Melbourne, St. Vincent’s Hospital, Melbourne, Australia
      name:Faculty of Health Sciences, Australian Catholic University, Melbourne, Australia
      name:Department of Pharmacology, University of Cambridge, Cambridge, UK
      name:Department of Pharmacology, University of Cambridge, Cambridge, UK

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