{"@context":{"@vocab":"https://cir.nii.ac.jp/schema/1.0/","rdfs":"http://www.w3.org/2000/01/rdf-schema#","dc":"http://purl.org/dc/elements/1.1/","dcterms":"http://purl.org/dc/terms/","foaf":"http://xmlns.com/foaf/0.1/","prism":"http://prismstandard.org/namespaces/basic/2.0/","cinii":"http://ci.nii.ac.jp/ns/1.0/","datacite":"https://schema.datacite.org/meta/kernel-4/","ndl":"http://ndl.go.jp/dcndl/terms/","jpcoar":"https://github.com/JPCOAR/schema/blob/master/2.0/"},"@id":"https://cir.nii.ac.jp/crid/1362825894771545344.json","@type":"Article","productIdentifier":[{"identifier":{"@type":"DOI","@value":"10.1152/ajprenal.00030.2009"}},{"identifier":{"@type":"URI","@value":"https://www.physiology.org/doi/pdf/10.1152/ajprenal.00030.2009"}}],"dc:title":[{"@value":"Expression and phosphorylation of the Na<sup>+</sup>-Cl<sup>−</sup> cotransporter NCC in vivo is regulated by dietary salt, potassium, and SGK1"}],"description":[{"type":"abstract","notation":[{"@value":"<jats:p> The Na-Cl cotransporter NCC is expressed in the distal convoluted tubule, activated by phosphorylation, and has been implicated in renal NaCl and K<jats:sup>+</jats:sup> homeostasis. The serum and glucocorticoid inducible kinase 1 (SGK1) contributes to renal NaCl retention and K<jats:sup>+</jats:sup> excretion, at least in part, by stimulating the epithelial Na<jats:sup>+</jats:sup> channel and Na<jats:sup>+</jats:sup>-K<jats:sup>+</jats:sup>-ATPase in the downstream segments of aldosterone-sensitive Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup> exchange. In this study we confirmed in wild-type mice (WT) that dietary NaCl restriction increases renal NCC expression and its phosphorylation at Thr<jats:sup>53</jats:sup>, Thr<jats:sup>58</jats:sup>, and Ser<jats:sup>71</jats:sup>, respectively. This response, however, was attenuated in mice lacking SGK1 ( Sgk1<jats:sup>−/−</jats:sup>), which may contribute to impaired NaCl retention in those mice. Total renal NCC expression and phosphorylation at Thr<jats:sup>53</jats:sup>, Thr<jats:sup>58</jats:sup>, and Ser<jats:sup>71</jats:sup> in WT were greater under low- compared with high-K<jats:sup>+</jats:sup> diet. This finding is consistent with a regulation of NCC to modulate Na<jats:sup>+</jats:sup> delivery to downstream segments of Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup> exchange, thereby modulating K<jats:sup>+</jats:sup> excretion. Dietary K<jats:sup>+</jats:sup>-dependent variation in renal expression of total NCC and phosphorylated NCC were not attenuated in Sgk1<jats:sup>−/−</jats:sup> mice. In fact, high-K<jats:sup>+</jats:sup> diet-induced NCC suppression was enhanced in Sgk1<jats:sup>−/−</jats:sup> mice. The hyperkalemia induced in Sgk1<jats:sup>−/−</jats:sup> mice by a high-K<jats:sup>+</jats:sup> diet may have augmented NCC suppression, thereby increasing Na<jats:sup>+</jats:sup> delivery and facilitating K<jats:sup>+</jats:sup> excretion in downstream segments of impaired Na<jats:sup>+</jats:sup>/K<jats:sup>+</jats:sup> exchange. In summary, changes in NaCl and K<jats:sup>+</jats:sup> intake altered NCC expression and phosphorylation, an observation consistent with a role of NCC in NaCl and K<jats:sup>+</jats:sup> homeostasis. The two maneuvers dissociated plasma aldosterone levels from NCC expression and phosphorylation, implicating additional regulators. Regulation of NCC expression and phosphorylation by dietary NaCl restriction appears to involve SGK1. </jats:p>"}]}],"creator":[{"@id":"https://cir.nii.ac.jp/crid/1382825894771545348","@type":"Researcher","foaf:name":[{"@value":"Volker Vallon"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894771545344","@type":"Researcher","foaf:name":[{"@value":"Jana Schroth"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894771545345","@type":"Researcher","foaf:name":[{"@value":"Florian Lang"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894771545346","@type":"Researcher","foaf:name":[{"@value":"Dietmar Kuhl"}]},{"@id":"https://cir.nii.ac.jp/crid/1382825894771545347","@type":"Researcher","foaf:name":[{"@value":"Shinichi Uchida"}]}],"publication":{"publicationIdentifier":[{"@type":"PISSN","@value":"1931857X"},{"@type":"EISSN","@value":"15221466"}],"prism:publicationName":[{"@value":"American Journal of Physiology-Renal Physiology"}],"dc:publisher":[{"@value":"American Physiological Society"}],"prism:publicationDate":"2009-09","prism:volume":"297","prism:number":"3","prism:startingPage":"F704","prism:endingPage":"F712"},"reviewed":"false","url":[{"@id":"https://www.physiology.org/doi/pdf/10.1152/ajprenal.00030.2009"}],"createdAt":"2009-07-02","modifiedAt":"2019-09-09","relatedProduct":[{"@id":"https://cir.nii.ac.jp/crid/1360002215822810752","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"Effect of angiotensin II on the WNK-OSR1/SPAK-NCC phosphorylation cascade in cultured mpkDCT cells and in vivo mouse kidney"}]},{"@id":"https://cir.nii.ac.jp/crid/1360002216923031168","@type":"Article","resourceType":"学術雑誌論文(journal article)","relationType":["isReferencedBy"],"jpcoar:relatedTitle":[{"@value":"WNK4 is the major WNK positively regulating NCC in the mouse kidney"}]},{"@id":"https://cir.nii.ac.jp/crid/1360283694068020736","@type":"Article","resourceType":"学術雑誌論文(journal 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