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Article: Insignificant effect of secretin in rodent models of polycystic kidney and liver disease

TitleInsignificant effect of secretin in rodent models of polycystic kidney and liver disease
Authors
KeywordsAutosomal Dominant Polycystic Kidney Disease
Cyclic Amp
Polycystic Kidney Disease
Secretin
Secretin Receptor
Vasopressin
Issue Date2012
Citation
American Journal Of Physiology - Renal Physiology, 2012, v. 303 n. 7, p. F1089-F1098 How to Cite?
AbstractPolycystic kidney (PKD) and liver (PLD) diseases cause significant morbidity and mortality. A large body of evidence indicates that cyclic AMP plays an important role in their pathogenesis. Clinical trials of drugs that reduce cyclic AMP levels in target tissues are now in progress. Secretin may contribute to adenylyl cyclase-dependent urinary concentration and is a major agonist of adenylyl cyclase in cholangiocytes. To investigate the role of secretin in PKD and PLD, we have studied the expression of secretin and the secretin receptor in rodent models orthologous to autosomal recessive (PCK rat) and dominant (Pkd2 -/WS25 mouse) PKD; the effects of exogenous secretin administration to PCK rats, PCK rats lacking circulating vasopressin (PCK di/di), and Pkd2 /WS25 mice; and the impact of a nonfunctional secretin receptor on disease development in Pkd2 -/WS25:SCTR -/-double mutants. Renal and hepatic secretin and secretin receptor mRNA and plasma secretin were increased in both models, and secretin receptor protein was increased in the kidneys and liver of Pkd2 -/WS25 mice. However, exogenous secretin administered subcutaneously via osmotic pumps had minimal or negligible effects and the absence of a functional secretin receptor had no influence on the severity of PKD or PLD. Therefore, it is unlikely that by itself secretin plays a significant role in the pathogenesis of PKD and/or PLD. © 2012 the American Physiological Society.
Persistent Identifierhttp://hdl.handle.net/10722/179318
ISSN
2008 Impact Factor: 3.89
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorWang, Xen_US
dc.contributor.authorYe, Hen_US
dc.contributor.authorWard, CJen_US
dc.contributor.authorChu, JYSen_US
dc.contributor.authorMasyuk, TVen_US
dc.contributor.authorLarusso, NFen_US
dc.contributor.authorHarris, PCen_US
dc.contributor.authorChow, BKCen_US
dc.contributor.authorTorres, VEen_US
dc.date.accessioned2012-12-19T09:54:07Z-
dc.date.available2012-12-19T09:54:07Z-
dc.date.issued2012en_US
dc.identifier.citationAmerican Journal Of Physiology - Renal Physiology, 2012, v. 303 n. 7, p. F1089-F1098en_US
dc.identifier.issn0363-6127en_US
dc.identifier.urihttp://hdl.handle.net/10722/179318-
dc.description.abstractPolycystic kidney (PKD) and liver (PLD) diseases cause significant morbidity and mortality. A large body of evidence indicates that cyclic AMP plays an important role in their pathogenesis. Clinical trials of drugs that reduce cyclic AMP levels in target tissues are now in progress. Secretin may contribute to adenylyl cyclase-dependent urinary concentration and is a major agonist of adenylyl cyclase in cholangiocytes. To investigate the role of secretin in PKD and PLD, we have studied the expression of secretin and the secretin receptor in rodent models orthologous to autosomal recessive (PCK rat) and dominant (Pkd2 -/WS25 mouse) PKD; the effects of exogenous secretin administration to PCK rats, PCK rats lacking circulating vasopressin (PCK di/di), and Pkd2 /WS25 mice; and the impact of a nonfunctional secretin receptor on disease development in Pkd2 -/WS25:SCTR -/-double mutants. Renal and hepatic secretin and secretin receptor mRNA and plasma secretin were increased in both models, and secretin receptor protein was increased in the kidneys and liver of Pkd2 -/WS25 mice. However, exogenous secretin administered subcutaneously via osmotic pumps had minimal or negligible effects and the absence of a functional secretin receptor had no influence on the severity of PKD or PLD. Therefore, it is unlikely that by itself secretin plays a significant role in the pathogenesis of PKD and/or PLD. © 2012 the American Physiological Society.en_US
dc.languageengen_US
dc.relation.ispartofAmerican Journal of Physiology - Renal Physiologyen_US
dc.subjectAutosomal Dominant Polycystic Kidney Diseaseen_US
dc.subjectCyclic Ampen_US
dc.subjectPolycystic Kidney Diseaseen_US
dc.subjectSecretinen_US
dc.subjectSecretin Receptoren_US
dc.subjectVasopressinen_US
dc.titleInsignificant effect of secretin in rodent models of polycystic kidney and liver diseaseen_US
dc.typeArticleen_US
dc.identifier.emailChu, JYS: hitan@graduate.hku.hken_US
dc.identifier.emailChow, BKC: bkcc@hku.hken_US
dc.identifier.authorityChu, JYS=rp00684en_US
dc.identifier.authorityChow, BKC=rp00681en_US
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1152/ajprenal.00242.2012en_US
dc.identifier.pmid22811488-
dc.identifier.scopuseid_2-s2.0-84867115802en_US
dc.identifier.hkuros222855-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-84867115802&selection=ref&src=s&origin=recordpageen_US
dc.identifier.volume303en_US
dc.identifier.issue7en_US
dc.identifier.spageF1089en_US
dc.identifier.epageF1098en_US
dc.identifier.isiWOS:000309512400020-
dc.identifier.scopusauthoridWang, X=36716978500en_US
dc.identifier.scopusauthoridYe, H=36887037900en_US
dc.identifier.scopusauthoridWard, CJ=35785364400en_US
dc.identifier.scopusauthoridChu, JYS=34975209300en_US
dc.identifier.scopusauthoridMasyuk, TV=6508281360en_US
dc.identifier.scopusauthoridLarusso, NF=35391955800en_US
dc.identifier.scopusauthoridHarris, PC=24539364700en_US
dc.identifier.scopusauthoridChow, BKC=7102826193en_US
dc.identifier.scopusauthoridTorres, VE=7102165897en_US

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