2018
Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization.
Memi F, Tirziu D, Papangeli I. Tissue-specific miRNA Expression Profiling in Mouse Heart Sections Using In Situ Hybridization. Journal Of Visualized Experiments 2018 PMID: 30272664, PMCID: PMC6235194, DOI: 10.3791/57920.Peer-Reviewed Original ResearchConceptsMouse heart sectionsMiRNA expression profilingMiRNA-182Relevant protein expressionMiRNAs of interestMiRNA transcriptsT proteinRNA transcriptsExpression profilingMicro-RNAsDetailed protocolSitu hybridization techniqueCardiac troponin T proteinsSitu hybridizationLNA probesProtein expressionTroponin T proteinsTranscriptsHybridization techniqueCardiomyocyte cellsProteinExpressionFluorescent stainingMiRNA detectionRNAs
2016
miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor