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dc.contributor.authorEdwards, Aurelieen_US
dc.contributor.authorLayton, Anita T.en_US
dc.date.accessioned2020-03-02T14:42:23Z
dc.date.available2020-03-02T14:42:23Z
dc.date.issued2017-11-01
dc.identifierhttp://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcApp=PARTNER_APP&SrcAuth=LinksAMR&KeyUT=WOS:000414148000004&DestLinkType=FullRecord&DestApp=ALL_WOS&UsrCustomerID=6e74115fe3da270499c3d65c9b17d654
dc.identifier.citationAurelie Edwards, Anita T Layton. 2017. "Cell Volume Regulation in the Proximal Tubule of Rat Kidney Proximal Tubule Cell Volume Regulation." BULLETIN OF MATHEMATICAL BIOLOGY, Volume 79, Issue 11, pp. 2512 - 2533. https://doi.org/10.1007/s11538-017-0338-6
dc.identifier.issn0092-8240
dc.identifier.issn1522-9602
dc.identifier.urihttps://hdl.handle.net/2144/39596
dc.description.abstractWe developed a dynamic model of a rat proximal convoluted tubule cell in order to investigate cell volume regulation mechanisms in this nephron segment. We examined whether regulatory volume decrease (RVD), which follows exposure to a hyposmotic peritubular solution, can be achieved solely via stimulation of basolateral K^+ and Cl^− channels and Na^+–HCO₃^− cotransporters. We also determined whether regulatory volume increase (RVI), which follows exposure to a hyperosmotic peritubular solution under certain conditions, may be accomplished by activating basolateral Na^+/H^+ exchangers. Model predictions were in good agreement with experimental observations in mouse proximal tubule cells assuming that a 10% increase in cell volume induces a fourfold increase in the expression of basolateral K+ and Cl− channels and Na+–HCO₃^− cotransporters. Our results also suggest that in response to a hyposmotic challenge and subsequent cell swelling, Na^+–HCO₃^− cotransporters are more efficient than basolateral K^+ and Cl^− channels at lowering intracellular osmolality and reducing cell volume. Moreover, both RVD and RVI are predicted to stabilize net transcellular Na^+ reabsorption, that is, to limit the net Na^+ flux decrease during a hyposmotic challenge or the net Na^+ flux increase during a hyperosmotic challenge.en_US
dc.description.sponsorshipThis research was supported by the National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, via grant R01DK106102 to AT Layton. (R01DK106102 - National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases)en_US
dc.format.extentp. 2512 - 2533en_US
dc.languageEnglish
dc.language.isoen_US
dc.publisherSPRINGERen_US
dc.relation.ispartofBULLETIN OF MATHEMATICAL BIOLOGY
dc.subjectScience & technologyen_US
dc.subjectLife sciences & biomedicineen_US
dc.subjectBiologyen_US
dc.subjectMathematical & computational biologyen_US
dc.subjectCell volume regulationen_US
dc.subjectOsmotic challengeen_US
dc.subjectProximal tubuleen_US
dc.subjectMathematical modelen_US
dc.subjectPotassium conductanceen_US
dc.subjectMathematical-modelen_US
dc.subjectOxygen-consumptionen_US
dc.subjectConvoluted tubuleen_US
dc.subjectPrimary culturesen_US
dc.subjectStraight tubuleen_US
dc.subjectP-glycoproteinen_US
dc.subjectHomeostasisen_US
dc.subjectMechanismsen_US
dc.subjectTransporten_US
dc.subjectAnimalsen_US
dc.subjectCell sizeen_US
dc.subjectComputer simulationen_US
dc.subjectIon channelsen_US
dc.subjectKidney tubules, proximalen_US
dc.subjectMathematical conceptsen_US
dc.subjectModels, biologicalen_US
dc.subjectOsmoregulationen_US
dc.subjectRatsen_US
dc.subjectMathematical sciencesen_US
dc.subjectBiological sciencesen_US
dc.subjectBioinformaticsen_US
dc.titleCell volume regulation in the proximal tubule of rat kidney proximal tubule cell volume regulationen_US
dc.typeArticleen_US
dc.description.versionAccepted manuscripten_US
dc.identifier.doi10.1007/s11538-017-0338-6
pubs.elements-sourceweb-of-scienceen_US
pubs.notesEmbargo: Not knownen_US
pubs.organisational-groupBoston Universityen_US
pubs.organisational-groupBoston University, College of Engineeringen_US
pubs.organisational-groupBoston University, College of Engineering, Department of Biomedical Engineeringen_US
pubs.publication-statusPublisheden_US
dc.identifier.mycv283163


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