2015
Polycystin-1 Is a Cardiomyocyte Mechanosensor That Governs L-Type Ca2+ Channel Protein Stability
Pedrozo Z, Criollo A, Battiprolu PK, Morales CR, Contreras-Ferrat A, Fernández C, Jiang N, Luo X, Caplan MJ, Somlo S, Rothermel BA, Gillette TG, Lavandero S, Hill JA. Polycystin-1 Is a Cardiomyocyte Mechanosensor That Governs L-Type Ca2+ Channel Protein Stability. Circulation 2015, 131: 2131-2142. PMID: 25888683, PMCID: PMC4470854, DOI: 10.1161/circulationaha.114.013537.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornBiomarkersCalcium Channels, L-TypeCardiomegalyCells, CulturedFibrosisHypertrophyHypotonic SolutionsMaleMechanotransduction, CellularMiceMice, KnockoutMyocytes, CardiacProtein Interaction MappingProtein StabilityProtein Structure, TertiaryRatsRats, Sprague-DawleyRecombinant Fusion ProteinsRNA InterferenceStress, MechanicalTRPP Cation ChannelsConceptsL-type calcium channel activityCalcium channel activityNeonatal rat ventricular myocytesRat ventricular myocytesKnockout miceVentricular myocytesChannel activityMechanical stretchNeonatal rat ventricular myocyte hypertrophyProtein levelsVentricular myocyte hypertrophyL-type Ca2G protein-coupled receptor-like proteinPolycystin-1Channel protein levelsCyclic mechanical stretchControl miceInterstitial fibrosisStress-induced activationCardiac massMechanical stress-induced activationCardiac functionRNAi-dependent knockdownCardiac hypertrophyLittermate controls
2013
Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation
Pluznick JL, Protzko RJ, Gevorgyan H, Peterlin Z, Sipos A, Han J, Brunet I, Wan LX, Rey F, Wang T, Firestein SJ, Yanagisawa M, Gordon JI, Eichmann A, Peti-Peterdi J, Caplan MJ. Olfactory receptor responding to gut microbiota-derived signals plays a role in renin secretion and blood pressure regulation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2013, 110: 4410-4415. PMID: 23401498, PMCID: PMC3600440, DOI: 10.1073/pnas.1215927110.Peer-Reviewed Original ResearchConceptsShort-chain fatty acidsRenin secretionBlood pressureGut microbiotaG protein-coupled receptor 41Acute hypotensive responseRenal juxtaglomerular apparatusSmall resistance vesselsMicrobiota-derived signalsModulate blood pressureBlood pressure regulationWild-type miceSmooth muscle cellsG protein-coupled receptorsGPR41 expressionOlfactory receptorsHypotensive responseProtein-coupled receptorsSCFA receptorsResistance vesselsJuxtaglomerular apparatusAntibiotic treatmentOlfr78Receptor 41Knockout mice
2012
AS160: a new Na,K‐ATPase partner that regulates the trafficking of the sodium pump in response to energy depletion and renal ischemia
Alves D, Thulin G, Loffing J, Kashgarian M, Caplan M. AS160: a new Na,K‐ATPase partner that regulates the trafficking of the sodium pump in response to energy depletion and renal ischemia. The FASEB Journal 2012, 26: lb808-lb808. DOI: 10.1096/fasebj.26.1_supplement.lb808.Peer-Reviewed Original ResearchPlasma membraneRenal epithelial cellsK-ATPaseEpithelial cellsCytoplasmic vesicular compartmentsDifferent cellular poolsCultured epithelial cellsVesicular compartmentsWild typeCellular poolAS160Cytoplasmic accumulationKnockout micePhysiological roleWild-type controlsEnergy depletionRenal ischemiaPhysiological stimuliType controlsCellular NaK-ATPase activityIntracellular accumulationMembraneIschemic kidney injuryCells
2010
Exosome‐release of beta‐catenin: A novel mechanism to antagonize Wnt signaling
Chairoungdua A, Smith D, Pochard P, Hull M, Caplan M. Exosome‐release of beta‐catenin: A novel mechanism to antagonize Wnt signaling. The FASEB Journal 2010, 24: 715.3-715.3. DOI: 10.1096/fasebj.24.1_supplement.715.3.Peer-Reviewed Original ResearchWnt/β-cateninWnt/β-catenin activityDendritic cellsΒ-cateninΒ-catenin activityCD9 expressionE-cadherinTumor metastasisWild-type miceNovel mechanismΒ-catenin protein levelsT cellsΒ-catenin levelsKnockout miceTumor cell metastasisCell metastasisGSK-3βMetastasisCHO cellsLuciferase reporterInappropriate activationCD82 expressionProtein levelsHEK 293T cellsSignificant decrease