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showing 10 items of 16837 documents

Cardiomyocyte proliferation prevents failure in pressure overload but not volume overload

2017

Induction of the cell cycle is emerging as an intervention to treat heart failure. Here, we tested the hypothesis that enhanced cardiomyocyte renewal in transgenic mice expressing cyclin D2 would be beneficial during hemodynamic overload. We induced pressure overload by transthoracic aortic constriction (TAC) or volume overload by aortocaval shunt in cyclin D2-expressing and WT mice. Although cyclin D2 expression dramatically improved survival following TAC, it did not confer a survival advantage to mice following aortocaval shunt. Cardiac function decreased following TAC in WT mice, but was preserved in cyclin D2-expressing mice. On the other hand, cardiac structure and function were compr…

0301 basic medicineCardiac function curvemedicine.medical_specialtyAortic DiseasesVolume overloadCardiomegalyMice TransgenicConstriction Pathologic030204 cardiovascular system & hematologyMice03 medical and health sciences0302 clinical medicineCyclin D2FibrosisInternal medicinemedicineAnimalsCyclin D2Myocytes CardiacCell ProliferationCyclinHeart FailurePressure overloadbusiness.industryGeneral MedicineCell cyclemedicine.disease030104 developmental biologyEndocrinologyHeart failurebusinessResearch ArticleJournal of Clinical Investigation
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Guanxin Danshen Formulation Protects against Myocardial Ischemia Reperfusion Injury-Induced Left Ventricular Remodeling by Upregulating Estrogen Rece…

2017

Background: Guanxin Danshen formulation (GXDSF) is a traditional Chinese herbal recipe recorded in the Chinese Pharmacopoeia since 1995 edition, which consists of Salviae miltiorrhizae Radix et Rhizoma, Notoginseng Radix et Rhizoma and Dalbergiae odoriferae Lignum. Our previous research suggested GXDSF had positive effect on cardiovascular disease. Therefore, the aim of this study was to elucidate the effects of GXDSF on myocardial ischemia reperfusion injury-induced left ventricular remodelling (MIRI-LVR). Methods: The effects of GXDSF on cardiac function were detected by haemodynamics and echocardiograms. The effects of GXDSF on biochemical parameters (AST, LDH and CK-MB) were analysed. H…

0301 basic medicineCardiac function curvemedicine.medical_specialtyGuanxin Danshen formulaEstrogen receptor030204 cardiovascular system & hematologyPharmacologyventricular remodeling03 medical and health sciences0302 clinical medicineFibrosisInternal medicinemedicinenetwork pharmacologyPharmacology (medical)Ventricular remodelingOriginal ResearchPharmacologyPI3K/AktEjection fractionbusiness.industryestrogen receptor βlcsh:RM1-950PHTPPmedicine.diseasemyocardial ischemia reperfusion injury030104 developmental biologylcsh:Therapeutics. PharmacologyCardiologyMyocardial fibrosisbusinessReperfusion injuryFrontiers in Pharmacology
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Protective Role for LPA3 in Cardiac Hypertrophy Induced by Myocardial Infarction but Not by Isoproterenol

2017

Background: We previously reported that lysophosphatidic acid (LPA) promoted cardiomyocyte hypertrophy in vitro via one of its G protein-coupled receptor subtypes, LPA3. In this study, we examined the role of LPA3 in cardiac hypertrophy induced by isoproterenol (ISO) and myocardial infarction. Methods: In vitro, neonatal rat cardiomyocytes (NRCMs) were subjected to LPA3 knocked-down, or pretreated with a β-adrenergic receptor (β-AR) antagonist (propranolol) before LPA/ISO treatment. Cardiomyocyte size and hypertrophic gene (ANP, BNP) mRNA levels were determined. In vivo, LPA3-/- and wild-type mice were implanted subcutaneously with an osmotic mini-pump containing ISO or vehicle for 2 weeks;…

0301 basic medicineCardiac function curvemedicine.medical_specialtyPhysiologyIschemiaInfarctionPropranolol030204 cardiovascular system & hematologylcsh:PhysiologyMuscle hypertrophy03 medical and health scienceschemistry.chemical_compound0302 clinical medicineIn vivoPhysiology (medical)Internal medicineLysophosphatidic acidmedicineMyocardial infarctionOriginal ResearchMIlcsh:QP1-981business.industryisoproterenolLPA3medicine.disease030104 developmental biologyEndocrinologychemistrybusinesshypertrophylysophosphatidic acidmedicine.drugFrontiers in Physiology
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Homozygous Resistance to Thyroid Hormone β: Can Combined Antithyroid Drug and Triiodothyroacetic Acid Treatment Prevent Cardiac Failure?

2017

Resistance to thyroid hormone β (RTHβ) due to homozygous THRB defects is exceptionally rare, with only five kindreds reported worldwide. Cardiac dysfunction, which can be life-threatening, is recognized in the disorder. Here we describe the clinical, metabolic, ophthalmic, and cardiac findings in a 9-year-old boy harboring a biallelic THRB mutation (R243Q), along with biochemical, physiologic, and cardiac responses to carbimazole and triiodothyroacetic acid (TRIAC) therapy. The patient exhibits recognized features (goiter, nonsuppressed thyroid-stimulating hormone levels, upper respiratory tract infections, hyperactivity, low body mass index) of heterozygous RTHβ, with additional characteri…

0301 basic medicineCardiac function curvemedicine.medical_specialtyendocrine systemGoiterendocrine system diseasesEndocrinology Diabetes and Metabolism030209 endocrinology & metabolismCase ReportsCardiovascularthyroidresistance to thyroid hormonehomozygous THRB mutation03 medical and health sciences0302 clinical medicineClinical ResearchInternal medicinemedicine2.1 Biological and endogenous factorsDecompensation2. Zero hungercardiac thyrotoxicosisbusiness.industryThyroidDilated cardiomyopathymedicine.disease3. Good health030104 developmental biologyEndocrinologymedicine.anatomical_structureCarbimazoleHeart Disease6.1 PharmaceuticalsBasal metabolic ratebusinessHormonemedicine.drug
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mRNA-binding protein tristetraprolin is essential for cardiac response to iron deficiency by regulating mitochondrial function

2018

Cells respond to iron deficiency by activating iron-regulatory proteins to increase cellular iron uptake and availability. However, it is not clear how cells adapt to conditions when cellular iron uptake does not fully match iron demand. Here, we show that the mRNA-binding protein tristetraprolin (TTP) is induced by iron deficiency and degrades mRNAs of mitochondrial Fe/S-cluster-containing proteins, specifically Ndufs1 in complex I and Uqcrfs1 in complex III, to match the decrease in Fe/S-cluster availability. In the absence of TTP, Uqcrfs1 levels are not decreased in iron deficiency, resulting in nonfunctional complex III, electron leakage, and oxidative damage. Mice with deletion of Ttp …

0301 basic medicineCardiac responseCardiac function curveIron-Sulfur ProteinsTristetraprolinMitochondria HeartCell Line03 medical and health sciencesElectron Transport Complex IIIMiceTristetraprolinmedicineAnimalschemistry.chemical_classificationMice KnockoutReactive oxygen speciesMultidisciplinaryNDUFS1MyocardiumNADH DehydrogenaseIron deficiencyIron Deficienciesmedicine.diseaseCell biology030104 developmental biologychemistryPNAS PlusCoenzyme Q – cytochrome c reductaseOxidation-ReductionFunction (biology)
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Cardioprotection and natural polyphenols: An update of clinical and experimental studies

2018

Myocardial ischemia is the leading cause of death worldwide. Despite better outcomes with early coronary artery reperfusion strategies, morbidity and mortality remain significant. The principal myocardial hallmark of myocardial ischemia is cell death and the associated impairment of cardiac contractility. In this way, the use of extracts from medicinal plants versus synthetic drugs to mitigate post-ischemic damage constitutes an alternative. Despite their proven beneficial effects in cardiovascular disorders, the use of many plants is questioned. Our aim is to update the clinical and experimental studies about the actions of medicinal plants and polyphenol-enriched extracts against ischemia…

0301 basic medicineCardiotonic AgentsMyocardial ischemiaCIENCIAS MÉDICAS Y DE LA SALUDMyocardial IschemiaMEDLINE030204 cardiovascular system & hematologyFisiologíaNATURAL PRODUCTS03 medical and health sciencesISCHEMIA-REPERFUSIONCARDIOPROTECTION0302 clinical medicineWeb of knowledgeMITOCHONDRIAAnimalsHumansMedicineCardioprotective AgentMedicinal plantsBeneficial effectsCause of deathCardioprotectionClinical Trials as TopicTraditional medicinePlant Extractsbusiness.industryPolyphenolsfood and beveragesGeneral MedicineMedicina Básica030104 developmental biologybusinessFood Science
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An actin network dispatches ciliary GPCRs into extracellular vesicles to modulate signaling

2017

Signaling receptors dynamically exit cilia upon activation of signaling pathways such as Hedgehog. Here, we find that when activated G protein-coupled receptors (GPCRs) fail to undergo BBSome-mediated retrieval from cilia back into the cell, these GPCRs concentrate into membranous buds at the tips of cilia before release into extracellular vesicles named ectosomes. Unexpectedly, actin and the actin regulators drebrin and myosin 6 mediate ectosome release from the tip of cilia. Mirroring signal-dependent retrieval, signal-dependent ectocytosis is a selective and effective process that removes activated signaling molecules from cilia. Congruently, ectocytosis compensates for BBSome defects as…

0301 basic medicineCell signalingBBSome*myosin 6*GPCR*exosomes*HedgehogBiologyKidneyGeneral Biochemistry Genetics and Molecular BiologyArticleCell LineReceptors G-Protein-Coupled03 medical and health sciencesExtracellular VesiclesMice0302 clinical medicine*BBSomeAnimalsHumans*ciliaCiliaReceptors SomatostatinHedgehog*actinActinG protein-coupled receptorCilium*extracellular vesiclesHedgehog signaling pathwayActinsCell biology030104 developmental biologyMicroscopy Electron ScanningSignal transduction*drebrin030217 neurology & neurosurgerySignal Transduction
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Evaluation of Planar-Cell-Polarity Phenotypes in Ciliopathy Mouse Mutant Cochlea

2016

In recent years, primary cilia have emerged as key regulators in development and disease by influencing numerous signaling pathways. One of the earliest signaling pathways shown to be associated with ciliary function was the non-canonical Wnt signaling pathway, also referred to as planar cell polarity (PCP) signaling. One of the best places in which to study the effects of planar cell polarity (PCP) signaling during vertebrate development is the mammalian cochlea. PCP signaling disruption in the mouse cochlea disrupts cochlear outgrowth, cellular patterning and hair cell orientation, all of which are affected by cilia dysfunction. The goal of this protocol is to describe the analysis of PCP…

0301 basic medicineCell signalingGeneral Chemical EngineeringStereocilia (inner ear)Cochlear ductBiologyGeneral Biochemistry Genetics and Molecular BiologyStereociliaMice03 medical and health sciencesHair Cells AuditorymedicineAnimalsCochleaGeneral Immunology and MicrobiologyGeneral NeuroscienceCiliumWnt signaling pathwayCell PolarityCochlear DuctEmbryo Mammalianmedicine.diseaseImmunohistochemistryCiliopathiesCochleaCell biologyDisease Models AnimalCiliopathyPhenotype030104 developmental biologymedicine.anatomical_structureMicroscopy Electron ScanningMedicinesense organsHair cellSignal TransductionJournal of Visualized Experiments
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Conversion of Nonproliferating Astrocytes into Neurogenic Neural Stem Cells: Control by FGF2 and Interferon-gamma

2016

Abstract Conversion of astrocytes to neurons, via de-differentiation to neural stem cells (NSC), may be a new approach to treat neurodegenerative diseases and brain injuries. The signaling factors affecting such a cell conversion are poorly understood, and they are hard to identify in complex disease models or conventional cell cultures. To address this question, we developed a serum-free, strictly controlled culture system of pure and homogeneous “astrocytes generated from murine embryonic stem cells (ESC).” These stem cell derived astrocytes (mAGES), as well as standard primary astrocytes resumed proliferation upon addition of FGF. The signaling of FGF receptor tyrosine kinase converted G…

0301 basic medicineCell signalingNeurogenesisBiologyInterferon-gammaMice03 medical and health sciences0302 clinical medicineNeural Stem CellsNeurosphereddc:570medicineAnimalsCell ProliferationEpidermal Growth FactorMultipotent Stem CellsCell CycleNeurogenesisMouse Embryonic Stem CellsCell BiologyAnatomyCell DedifferentiationEmbryonic stem cellNeural stem cellCell biologyNeuroepithelial cell030104 developmental biologymedicine.anatomical_structureGene Expression RegulationAstrocytesMolecular MedicineFibroblast Growth Factor 2Stem cell030217 neurology & neurosurgerySignal TransductionDevelopmental BiologyAstrocyte
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Type 5 phosphodiesterase (PDE5) and the vascular tree: from embryogenesis to aging and disease

2020

Highlights • Vascular development depends on the timely differentiation of endothelial and smooth muscle cells, that mutually influence their developmental fate. • Endothelial and vascular smooth muscle cell (VSMC) compartments can mutually influence cell and tissue modifications during vascular aging and in vascular disease. • Keeping in mind that PDE5 is mainly expressed in VSMCs, we surveyed the literature on the role of PDE5 in vascular development, aging and disease. • Although most results have been obtained by PDE5 pharmacological inhibition, no data are available, to date, on vascular development, aging or disease following PDE5 genetic ablation.

0301 basic medicineCell typeAgingVascular smooth muscleMyocytes Smooth MuscleVSMCsEmbryonic DevelopmentECsContext (language use)DiseaseBiologyMuscle Smooth VascularArticle03 medical and health sciences0302 clinical medicinenitric oxidevascular smooth muscle cellsHumansBioresorbable vascular scaffoldCyclic Nucleotide Phosphodiesterases Type 5ECEmbryogenesisPhosphodiesteraseVascular agingCell biologycGMPSettore MED/23ECs; PDE5; VSMCs; cGMP; nitric oxide030104 developmental biologyVascular aging; vascular smooth muscle cells; phosphodiesterasePDE5phosphodiesterase030217 neurology & neurosurgeryFunction (biology)Developmental Biology
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