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Article: Phenotypes developed in secretin receptor-null mice indicated a role for secretin in regulating renal water reabsorption

TitlePhenotypes developed in secretin receptor-null mice indicated a role for secretin in regulating renal water reabsorption
Authors
Issue Date2007
PublisherAmerican Society for Microbiology.
Citation
Molecular And Cellular Biology, 2007, v. 27 n. 7, p. 2499-2511 How to Cite?
AbstractAquaporin 2 (AQP2) is responsible for regulating the concentration of urine in the collecting tubules of the kidney under the control of vasopressin (Vp). Studies using Vp-deficient Brattleboro rats, however, indicated the existence of substantial Vp-independent mechanisms for membrane insertion, as well as transcriptional regulation, of this water channel. The Vp-independent mechanism(s) is clinically relevant to patients with X-linked nephrogenic diabetes insipidus (NDI) by therapeutically bypassing the dysfunctional Vp receptor. On the basis of studies with secretin receptor-null (SCTR -/-) mice, we report here for the first time that mutation of the SCTR gene could lead to mild polydipsia and polyuria. Additionally, SCTR -/- mice were shown to have reduced renal expression of AQP2 and AQP4, as well as altered glomerular and tubular morphology, suggesting possible disturbances in the filtration and/or water reabsorption process in these animals. By using SCTR-/- mice as controls and comparing them with wild-type animals, we performed both in vivo and in vitro studies that demonstrated a role for secretin in stimulating (i) AQP2 translocation from intracellular vesicles to the plasma membrane in renal medullary tubules and (ii) expression of this water channel under hyperosmotic conditions. The present study therefore provides information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating NDI patients. Copyright © 2007, American Society for Microbiology. All Rights Reserved.
Persistent Identifierhttp://hdl.handle.net/10722/67894
ISSN
2015 Impact Factor: 4.427
2015 SCImago Journal Rankings: 3.806
PubMed Central ID
ISI Accession Number ID
References
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DC FieldValueLanguage
dc.contributor.authorChu, JYSen_HK
dc.contributor.authorChung, SCKen_HK
dc.contributor.authorLam, AKMen_HK
dc.contributor.authorTam, Sen_HK
dc.contributor.authorChung, SKen_HK
dc.contributor.authorChow, BKCen_HK
dc.date.accessioned2010-09-06T05:59:14Z-
dc.date.available2010-09-06T05:59:14Z-
dc.date.issued2007en_HK
dc.identifier.citationMolecular And Cellular Biology, 2007, v. 27 n. 7, p. 2499-2511en_HK
dc.identifier.issn0270-7306en_HK
dc.identifier.urihttp://hdl.handle.net/10722/67894-
dc.description.abstractAquaporin 2 (AQP2) is responsible for regulating the concentration of urine in the collecting tubules of the kidney under the control of vasopressin (Vp). Studies using Vp-deficient Brattleboro rats, however, indicated the existence of substantial Vp-independent mechanisms for membrane insertion, as well as transcriptional regulation, of this water channel. The Vp-independent mechanism(s) is clinically relevant to patients with X-linked nephrogenic diabetes insipidus (NDI) by therapeutically bypassing the dysfunctional Vp receptor. On the basis of studies with secretin receptor-null (SCTR -/-) mice, we report here for the first time that mutation of the SCTR gene could lead to mild polydipsia and polyuria. Additionally, SCTR -/- mice were shown to have reduced renal expression of AQP2 and AQP4, as well as altered glomerular and tubular morphology, suggesting possible disturbances in the filtration and/or water reabsorption process in these animals. By using SCTR-/- mice as controls and comparing them with wild-type animals, we performed both in vivo and in vitro studies that demonstrated a role for secretin in stimulating (i) AQP2 translocation from intracellular vesicles to the plasma membrane in renal medullary tubules and (ii) expression of this water channel under hyperosmotic conditions. The present study therefore provides information for at least one of the Vp-independent mechanisms that modulate the process of renal water reabsorption. Future investigations in this direction should be important in developing therapeutic means for treating NDI patients. Copyright © 2007, American Society for Microbiology. All Rights Reserved.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Microbiology.en_HK
dc.relation.ispartofMolecular and Cellular Biologyen_HK
dc.rightsMolecular and Cellular Biology. Copyright © American Society for Microbiology.en_HK
dc.subject.meshAmino Acid Sequenceen_HK
dc.subject.meshAnimalsen_HK
dc.subject.meshAquaporin 2 - metabolismen_HK
dc.subject.meshAquaporin 4 - metabolismen_HK
dc.subject.meshBiological Transport, Activeen_HK
dc.subject.meshCell Membrane - metabolismen_HK
dc.subject.meshCytoplasmic Vesicles - metabolismen_HK
dc.subject.meshKidney Glomerulus - metabolism - pathologyen_HK
dc.subject.meshKidney Tubules - metabolism - pathologyen_HK
dc.subject.meshMiceen_HK
dc.subject.meshMice, Knockouten_HK
dc.subject.meshMolecular Sequence Dataen_HK
dc.subject.meshMutationen_HK
dc.subject.meshPhenotypeen_HK
dc.subject.meshPolyuria - genetics - physiopathologyen_HK
dc.subject.meshProtein Transporten_HK
dc.subject.meshRatsen_HK
dc.subject.meshReceptors, G-Protein-Coupled - genetics - physiologyen_HK
dc.subject.meshReceptors, Gastrointestinal Hormone - genetics - physiologyen_HK
dc.subject.meshSecretin - blood - physiologyen_HK
dc.subject.meshWater - metabolismen_HK
dc.titlePhenotypes developed in secretin receptor-null mice indicated a role for secretin in regulating renal water reabsorptionen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=0270-7306&volume=27&spage=2499&epage=2511&date=2007&atitle=Phenotypes+Developed+in+Secretin+Receptor-Null+Mice+Indicated+a+Role+for+Secretin+in+Regulating+Renal+Water+Reabsorptionen_HK
dc.identifier.emailChu, JYS: hitan@graduate.hku.hken_HK
dc.identifier.emailChung, SK: skchung@hkucc.hku.hken_HK
dc.identifier.emailChow, BKC: bkcc@hku.hken_HK
dc.identifier.authorityChu, JYS=rp00684en_HK
dc.identifier.authorityChung, SK=rp00381en_HK
dc.identifier.authorityChow, BKC=rp00681en_HK
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1128/MCB.01088-06en_HK
dc.identifier.pmid17283064-
dc.identifier.pmcidPMC1899889-
dc.identifier.scopuseid_2-s2.0-34147194125en_HK
dc.identifier.hkuros126294en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-34147194125&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume27en_HK
dc.identifier.issue7en_HK
dc.identifier.spage2499en_HK
dc.identifier.epage2511en_HK
dc.identifier.eissn1098-5549-
dc.identifier.isiWOS:000245410500008-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectA conditional knockout animal model for secretin-
dc.relation.projectSecretin: a putative neurosecretory hormone that regulates water homeostasis in the hypothalamus-pituitary-adrenal axis-
dc.identifier.scopusauthoridChu, JYS=34975209300en_HK
dc.identifier.scopusauthoridChung, SCK=35073685000en_HK
dc.identifier.scopusauthoridLam, AKM=7201848036en_HK
dc.identifier.scopusauthoridTam, S=7202037323en_HK
dc.identifier.scopusauthoridChung, SK=7404292976en_HK
dc.identifier.scopusauthoridChow, BKC=7102826193en_HK

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