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dc.creatorHéctor Chapoy Villanueva
dc.creatorGuillermo Torre Amione
dc.creatorGerardo de Jesús García Rivas
dc.creatorMaría Yuriana Oropeza Almazán
dc.date2017
dc.date.accessioned2018-10-18T22:08:20Z
dc.date.available2018-10-18T22:08:20Z
dc.identifier.issn19420900
dc.identifier.doi10.1155/2017/5750897
dc.identifier.urihttp://hdl.handle.net/11285/630561
dc.descriptionIntracellular Ca2+ mishandling is an underlying mechanism in hypoxia/reoxygenation (H/R) injury that results in mitochondrial dysfunction and cardiomyocytes death. These events are mediated by mitochondrial Ca2+ (mCa2+) overload that is facilitated by the mitochondrial calcium uniporter (MCU) channel. Along this line, we evaluated the effect of siRNA-targeting MCU in cardiomyocytes subjected to H/R injury. First, cardiomyocytes treated with siRNA demonstrated a reduction of MCU expression by 67%, which resulted in significant decrease in mitochondrial Ca2+ transport. siRNA treated cardiomyocytes showed decreased mitochondrial permeability pore opening and oxidative stress trigger by Ca2+ overload. Furthermore, after H/R injury MCU silencing decreased necrosis and apoptosis levels by 30% and 50%, respectively, and resulted in reduction in caspases 3/7, 9, and 8 activity. Our findings are consistent with previous conclusions that demonstrate that MCU activity is partly responsible for cellular injury induced by H/R and support the concept of utilizing siRNA-targeting MCU as a potential therapeutic strategy. © 2017 Yuriana Oropeza-Almazán et al.
dc.languageeng
dc.publisherHindawi Limited
dc.relationhttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85015781648&doi=10.1155%2f2017%2f5750897&partnerID=40&md5=1069b9c7889ecb9f49f0b3726465e2aa
dc.relationInvestigadores
dc.relationEstudiantes
dc.rightsinfo:eu-repo/semantics/openAccess
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0
dc.sourceOxidative Medicine and Cellular Longevity
dc.subjectCell death
dc.subjectMicrocontrollers
dc.subjectCalcium overload
dc.subjectCell viability
dc.subjectCellular injury
dc.subjectIntracellular Ca
dc.subjectMitochondrial calcium uniporter
dc.subjectMitochondrial dysfunction
dc.subjectSmall interfering RNA
dc.subjectTherapeutic strategy
dc.subjectCalcium
dc.subjectcalcium
dc.subjectsmall interfering RNA
dc.subjectcalcium
dc.subjectcalcium channel
dc.subjectcyclosporin
dc.subjectmessenger RNA
dc.subjectmitochondrial calcium uniporter
dc.subjectreactive oxygen metabolite
dc.subjectsmall interfering RNA
dc.subjectanimal cell
dc.subjectanimal experiment
dc.subjectapoptosis
dc.subjectArticle
dc.subjectcardiac muscle cell
dc.subjectcell damage
dc.subjectcell viability
dc.subjectcontrolled study
dc.subjectcytotoxicity
dc.subjectflow cytometry
dc.subjectgene targeting
dc.subjecthypoxia
dc.subjectin vitro study
dc.subjectmitochondrial membrane potential
dc.subjectmitochondrial permeability
dc.subjectnonhuman
dc.subjectoxidative stress
dc.subjectrat
dc.subjectreoxygenation
dc.subjectreperfusion injury
dc.subjectWestern blotting
dc.subjectanimal
dc.subjectcardiac muscle cell
dc.subjectcell hypoxia
dc.subjectcell line
dc.subjectcell survival
dc.subjectchemistry
dc.subjectcytology
dc.subjectdrug effects
dc.subjectgenetics
dc.subjectmetabolism
dc.subjectmitochondrion
dc.subjectmyocardial ischemia reperfusion injury
dc.subjectpathology
dc.subjectRNA interference
dc.subjectCalcium
dc.subjectCells
dc.subjectNucleic Acids
dc.subjectAnimals
dc.subjectApoptosis
dc.subjectCalcium
dc.subjectCalcium Channels
dc.subjectCell Hypoxia
dc.subjectCell Line
dc.subjectCell Survival
dc.subjectCyclosporine
dc.subjectMembrane Potential, Mitochondrial
dc.subjectMitochondria
dc.subjectMyocardial Reperfusion Injury
dc.subjectMyocytes, Cardiac
dc.subjectOxidative Stress
dc.subjectRats
dc.subjectReactive Oxygen Species
dc.subjectRNA Interference
dc.subjectRNA, Messenger
dc.subjectRNA, Small Interfering
dc.subject.classification7 INGENIERÍA Y TECNOLOGÍA
dc.titleSmall Interfering RNA Targeting Mitochondrial Calcium Uniporter Improves Cardiomyocyte Cell Viability in Hypoxia/Reoxygenation Injury by Reducing Calcium Overload
dc.typeArtículo
dc.identifier.volume2017
refterms.dateFOA2018-10-18T22:08:20Z


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