2018
Polycystin-2-dependent control of cardiomyocyte autophagy
Criollo A, Altamirano F, Pedrozo Z, Schiattarella GG, Li DL, Rivera-Mejías P, Sotomayor-Flores C, Parra V, Villalobos E, Battiprolu PK, Jiang N, May HI, Morselli E, Somlo S, de Smedt H, Gillette TG, Lavandero S, Hill JA. Polycystin-2-dependent control of cardiomyocyte autophagy. Journal Of Molecular And Cellular Cardiology 2018, 118: 110-121. PMID: 29518398, DOI: 10.1016/j.yjmcc.2018.03.002.Peer-Reviewed Original ResearchConceptsAutosomal dominant polycystic kidney diseaseIntracellular CaCardiomyocyte autophagyAutophagic fluxBAPTA-AMDominant polycystic kidney diseaseStress-induced autophagySarcoplasmic reticulum CaPolycystic kidney diseasePolycystin-2Impaired autophagic fluxKidney diseaseKnockout miceConsiderable evidence pointsMTOR inhibitionReticulum CaExtracellular CaMultiple cell typesAutophagic activityAutophagy inductionHomeostasisAutophagyEvidence pointsAutophagic controlCell types
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
2012
Mechanoprotection by Polycystins against Apoptosis Is Mediated through the Opening of Stretch-Activated K2P Channels
Peyronnet R, Sharif-Naeini R, Folgering JH, Arhatte M, Jodar M, Boustany C, Gallian C, Tauc M, Duranton C, Rubera I, Lesage F, Pei Y, Peters DJ, Somlo S, Sachs F, Patel A, Honoré E, Duprat F. Mechanoprotection by Polycystins against Apoptosis Is Mediated through the Opening of Stretch-Activated K2P Channels. Cell Reports 2012, 1: 241-250. PMID: 22832196, PMCID: PMC3437542, DOI: 10.1016/j.celrep.2012.01.006.Peer-Reviewed Original ResearchMeSH KeywordsAcidosisActin CytoskeletonAnimalsApoptosisChlorocebus aethiopsCOS CellsCytoprotectionDocosahexaenoic AcidsGene Knockout TechniquesIon Channel GatingKidney Tubules, ProximalMechanotransduction, CellularMiceMice, KnockoutMutant ProteinsPotassium Channels, Tandem Pore DomainProtein SubunitsStress, MechanicalTRPP Cation ChannelsConceptsEpithelial cellsRenal epithelial cellsProximal convoluted tubule epithelial cellsAutosomal dominant polycystic kidney diseaseDominant polycystic kidney diseaseKidney disease statesTubule epithelial cellsPolycystic kidney diseaseHeart failureKidney diseaseImportant pathologiesDisease statesApoptotic cell deathTREK-2K2P channelsCell deathApoptosisCellsAtherosclerosisDiseasePathology