0000000000181519

AUTHOR

Erhe Gao

showing 3 related works from this author

Epigenetic upregulation of endogenous VEGF-A reduces myocardial infarct size in mice.

2014

“Epigenetherapy” alters epigenetic status of the targeted chromatin and modifies expression of the endogenous therapeutic gene. In this study we used lentiviral in vivo delivery of small hairpin RNA (shRNA) into hearts in a murine infarction model. shRNA complementary to the promoter of vascular endothelial growth factor (VEGF-A) was able to upregulate endogenous VEGF-A expression. Histological and multiphoton microscope analysis confirmed the therapeutic effect in the transduced hearts. Magnetic resonance imaging (MRI) showed in vivo that the infarct size was significantly reduced in the treatment group 14 days after the epigenetherapy. Importantly, we show that promoter-targeted shRNA upr…

MaleVascular Endothelial Growth Factor ASmall interfering RNAAnatomy and PhysiologyTranscription GeneticMyocardial InfarctionEndogenyCardiovascularCardiovascular SystemEpigenesis GeneticSmall hairpin RNAMiceMolecular cell biologyNucleic AcidsGene expressionProtein IsoformsRNA Small InterferingCyclic AMP Response Element-Binding ProteinPromoter Regions GeneticRegulation of gene expressionMultidisciplinaryChromosome BiologyQRGenomicsGene TherapyChromatinInterventional CardiologyCell biologyUp-RegulationVascular endothelial growth factor AMedicineEpigeneticsDNA modificationHistone modificationResearch ArticleTranscriptional ActivationDrugs and DevicesScienceDNA transcriptionBiologyDownregulation and upregulationGenomic MedicineGeneticsGene silencingAnimalsGene SilencingBiologyBase SequenceInverted Repeat Sequencesta1182Membrane ProteinsDNA MethylationPhosphoproteinsMolecular biologyMice Inbred C57BLRNAGene expressionPloS one
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Systemic blockade of ACVR2B ligands protects myocardium from acute ischemia-reperfusion injury

2019

Activin A and myostatin, members of the transforming growth factor (TGF)-β superfamily of secreted factors, are potent negative regulators of muscle growth, but their contribution to myocardial ischemia-reperfusion (IR) injury is not known. The aim of this study was to investigate if activin 2B (ACVR2B) receptor ligands contribute to myocardial IR injury. Mice were treated with soluble ACVR2B decoy receptor (ACVR2B-Fc) and subjected to myocardial ischemia followed by reperfusion for 6 or 24 h. Systemic blockade of ACVR2B ligands by ACVR2B-Fc was protective against cardiac IR injury, as evidenced by reduced infarcted area, apoptosis, and autophagy and better preserved LV systolic function fo…

MaleActivin Receptors Type IIiskemialihaksetSmad2 ProteinMyostatinPharmacologyMice0302 clinical medicineDrug DiscoverykasvutekijätMyocytes CardiacCardioprotection0303 health sciences318 Medical biotechnologybiologysydänactivins1184 Genetics developmental biology physiologyII RECEPTORS3. Good health030220 oncology & carcinogenesisMolecular MedicineOriginal ArticleSignal TransductionCardiac function curvegrowth differentiation factorsProgrammed cell deathBLOCKINGischemia-reperfusion injuryIschemiaMyocardial Reperfusion InjuryMASSta311103 medical and health sciencesMYOSTATIN-KNOCKOUTCARDIOPROTECTIONGeneticsmedicineAnimalsMolecular Biologylihassolut030304 developmental biologyPharmacologySKELETAL-MUSCLE GROWTHbusiness.industryMyocardiumFOLLISTATINMyostatinmedicine.diseaseACVR2BMice Inbred C57BLACTIVIN-AGDF11GDF11biology.protein3111 BiomedicineproteiinitbusinessReperfusion injuryDIFFERENTIATION FACTOR 11ACVR2BTranscription Factors
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Heart infarct in NOD-SCID mice: therapeutic vasculogenesis by transplantation of human CD34+ cells and low dose CD34+KDR+ cells

2004

Hematopoietic (Hem) and endothelial (End) lineages derive from a common progenitor cell, the hemangioblast: specifically, the human cord blood (CB) CD34+KDR+ cell fraction comprises primitive Hem and End cells, as well as hemangioblasts. In humans, the potential therapeutic role of Hem and End progenitors in ischemic heart disease is subject to intense investigation. Particularly, the contribution of these cells to angiogenesis and cardiomyogenesis in myocardial ischemia is not well established. In our studies, we induced myocardial infarct (MI) in the immunocompromised NOD-SCID mouse model, and monitored the effects of myocardial transplantation of human CB CD34+ cells on cardiac function.…

Vascular Endothelial Growth Factor AneoangiogenesisTime FactorsAngiogenesisCell TransplantationHeart VentriclesCD34Myocardial InfarctionAntigens CD34ApoptosisMice SCIDBiologySCIDPeripheral blood mononuclear cellBiochemistryCulture Media Serum-FreeSerum-FreeCell FusionMiceVasculogenesisMice Inbred NODparasitic diseasesGeneticsAnimalsHumansVentricular Functionendothelial precursorsCell LineageProgenitor cellAntigensMolecular Biologyneoangiogenesis endothelial precursors hematopoietic stem cellsHemodynamicsFetal BloodVascular Endothelial Growth Factor Receptor-2Coculture Techniqueshematopoietic stem cellsCulture MediaTransplantationAutocrine CommunicationCord bloodImmunologycardiovascular systemCancer researchHemangioblastInbred NODCD34neoangiogenesis; endothelial precursors; hematopoietic stem cells; Animals; Antigens CD34; Apoptosis; Autocrine Communication; Cell Fusion; Cell Lineage; Coculture Techniques; Culture Media Serum-Free; Fetal Blood; Heart Ventricles; Hemodynamics; Humans; Mice; Mice Inbred NOD; Mice SCID; Myocardial Infarction; Time Factors; Vascular Endothelial Growth Factor A; Vascular Endothelial Growth Factor Receptor-2; Ventricular Function; Cell Transplantation; Biotechnology; Biochemistry; Molecular Biology; GeneticsBiotechnology
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