Search results for "Myocytes"

showing 7 items of 117 documents

Can you blame cold feet on Epac (and Rap1A)? Focus on “Cyclic AMP-Rap1A signaling activates RhoA to induce α2C-adrenoceptor translocation to the cell…

2012

Intracellular signaling by the second messenger cyclic AMP (cAMP) activates the Ras-related small GTPase Rap1 through the guanine exchange factor Epac. This activation leads to effector protein interactions, activation, and biological responses in the vasculature, including vasorelaxation. In vascular smooth muscle cells derived from human dermal arterioles (microVSM), Rap1 selectively regulates expression of G protein-coupled α2C-adrenoceptors (α2C-ARs) through JNK-c-jun nuclear signaling. The α2C-ARs are generally retained in the trans-Golgi compartment and mobilize to the cell surface and elicit vasoconstriction in response to cellular stress. The present study used human microVSM to exa…

medicine.medical_specialtyRHOAPhysiologyMyocytes Smooth MuscleCellChromosomal translocationSmooth muscleReceptors Adrenergic alpha-2Internal medicineCyclic AMPmedicineAnimalsHumansReceptorbiologyrap1 GTP-Binding ProteinsArticlesCell Biologyα2c adrenoceptorCell biologyProtein Transportmedicine.anatomical_structureEndocrinologybiology.proteinmedicine.symptomrhoA GTP-Binding ProteinVasoconstrictionAmerican Journal of Physiology-Cell Physiology
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Potential role of the neuropeptide CGRP in the induction of differentiation of rat hepatic portal vein wall.

2005

The media of the rat hepatic portal vein is composed of an internal circular muscular layer (CL) and an external longitudinal muscular layer (LL). These two perpendicular layers differentiate progressively from mesenchymal cells within the first month after birth. In this paper, we studied the development of calcitonin gene-related peptide (CGRP) innervation during post-natal differentiation of the vessel. We show that CGRP innervation is already present around the vessel at birth in the future adventitia but far from the lumen of the vessel. Progressively, CGRP immunoreactive fibers reached first LL then CL. CL by itself become only innervated at day 14 after birth. This corresponds to the…

medicine.medical_specialtyVascular smooth musclePhysiologyCalcitonin Gene-Related PeptideRecombinant Fusion ProteinsImmunocytochemistryMyocytes Smooth MuscleGene ExpressionCalcitonin gene-related peptideBiologyTransfectionBiochemistryMuscle Smooth VascularCell LineMuscular layerCellular and Molecular NeuroscienceMiceEndocrinologyInternal medicineAdventitiaMyosinmedicineAnimalsHumansRats WistarLuciferasesPromoter Regions GeneticBinding SitesMyosin Heavy ChainsPortal VeinNeuropeptidesAge FactorsCell DifferentiationImmunohistochemistryRatsEndocrinologymedicine.anatomical_structureLiverConnective TissueDesminHepatic portal veinRabbitsPeptides
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Insulin resistance aggravates atherosclerosis by reducing vascular smooth muscle cell survival and increasing CX3CL1/CX3CR1 axis.

2014

Aims Insulin resistance (IR) is a major risk factor for cardiovascular disease and atherosclerosis. Life-threatening acute events are mainly due to rupture of unstable plaques, and the role of vascular smooth muscle cells (VSMCs) in this process in IR, Type 2 diabetes mellitus, and metabolic syndrome (T2DM/MetS) has not been fully addressed. Therefore, the role of VSMC survival in the generation of unstable plaques in T2DM/MetS and the involvement of inflammatory mediators was investigated. Methods and results Defective insulin receptor substrate 2 (IRS2)-mediated signalling produced insulin-resistant VSMCs with reduced survival, migration, and higher apoptosis than control cells. Silencing…

medicine.medical_specialtyVascular smooth musclePhysiologyCell Survivalmedicine.medical_treatmentMyocytes Smooth MuscleCX3C Chemokine Receptor 1InflammationMice TransgenicBiologyMuscle Smooth VascularInsulin resistanceApolipoproteins EPhysiology (medical)Internal medicinemedicineAnimalsHumansProtein kinase BPI3K/AKT/mTOR pathwayCells CulturedMice KnockoutChemokine CX3CL1Insulinmedicine.diseaseAtherosclerosisIRS2Mice Inbred C57BLAtheromaEndocrinologyDiabetes Mellitus Type 2cardiovascular systemReceptors Chemokinemedicine.symptomInsulin ResistanceCardiology and Cardiovascular MedicineSignal TransductionCardiovascular research
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Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling

2015

Cardiac hypertrophy accompanies many forms of heart disease, including ischemic disease, hypertension, heart failure, and valvular disease, and it is a strong predictor of increased cardiovascular morbidity and mortality. Deletion of bone marrow kinase in chromosome X (Bmx), an arterial nonreceptor tyrosine kinase, has been shown to inhibit cardiac hypertrophy in mice. This finding raised the possibility of therapeutic use of Bmx tyrosine kinase inhibitors, which we have addressed here by analyzing cardiac hypertrophy in gene-targeted mice deficient in Bmx tyrosine kinase activity. We found that angiotensin II (Ang II)-induced cardiac hypertrophy is significantly reduced in mice deficient i…

medicine.medical_specialtyendotheliumEndotheliumAngiogenesiscardiomyocyteCardiomegalyheartmTORC1030204 cardiovascular system & hematologyMitochondria Heart03 medical and health sciencesMice0302 clinical medicineInternal medicinemedicineAnimalsMyocytes Cardiac030304 developmental biologyMice Knockout0303 health sciencesMultidisciplinaryKinasebusiness.industryta1184Angiotensin IIBiological SciencesProtein-Tyrosine KinasesAngiotensin IImedicine.anatomical_structureEndocrinologyEtkcardiovascular systemCancer researchPhosphorylationCytokinesEndothelium VascularSignal transductionInflammation MediatorssignalingbusinessTyrosine kinaseSignal Transduction
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Cardiac pacemaker function of HCN4 channels in mice is confined to embryonic development and requires cyclic AMP.

2008

Important targets for cAMP signalling in the heart are hyperpolarization-activated and cyclic nucleotide-gated (HCN) channels that underlie the depolarizing 'pacemaker' current, I(f). We studied the role of I(f) in mice, in which binding of cAMP to HCN4 channels was abolished by a single amino-acid exchange (R669Q). Homozygous HCN4(R669Q/R669Q) mice die during embryonic development. Prior to E12, homozygous and heterozygous embryos display reduced heart rates and show no or attenuated responses to catecholaminergic stimulation. Adult heterozygous mice display normal heart rates at rest and during exercise. However, following beta-adrenergic stimulation, hearts exhibit pauses and sino-atrial…

medicine.medical_specialtymedicine.medical_treatmentCyclic Nucleotide-Gated Cation ChannelsEmbryonic DevelopmentStimulationMice TransgenicBiologyIn Vitro TechniquesGeneral Biochemistry Genetics and Molecular BiologyCardiac pacemakerArticleMiceHeart RatePregnancyInternal medicineHeart ratemedicineCyclic AMPHyperpolarization-Activated Cyclic Nucleotide-Gated ChannelsAnimalsMyocytes CardiacMolecular BiologyIon channelCells CulturedCatecholaminergicGeneral Immunology and MicrobiologyGeneral NeuroscienceEmbryogenesisDepolarizationEmbryoHeartMice Inbred C57BLEndocrinologyMutationFemaleThe EMBO journal
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The Sick Adipose Tissue: New Insights Into Defective Signaling and Crosstalk With the Myocardium

2021

Adipose tissue (AT) biology is linked to cardiovascular health since obesity is associated with cardiovascular disease (CVD) and positively correlated with excessive visceral fat accumulation. AT signaling to myocardial cells through soluble factors known as adipokines, cardiokines, branched-chain amino acids and small molecules like microRNAs, undoubtedly influence myocardial cells and AT function via the endocrine-paracrine mechanisms of action. Unfortunately, abnormal total and visceral adiposity can alter this harmonious signaling network, resulting in tissue hypoxia and monocyte/macrophage adipose infiltration occurring alongside expanded intra-abdominal and epicardial fat depots seen …

obesityEndocrinology Diabetes and MetabolismAdipokineAdipose tissueAdipose tissueMyocardiocytesInflammationContext (language use)ReviewBioinformaticsDiseases of the endocrine glands. Clinical endocrinologyCoronary artery diseasechemistry.chemical_compoundEndocrinologyAdipocytemicrobiotamedicineHumansMyocytes CardiacMyocardial infarctionObesityInflammationbusiness.industryMyocardiumMicrobiotaRC648-665medicine.diseaseCor MalaltiesmyocardiocytesAdipose TissuechemistryObesitatmedicine.symptombusinessDysbiosisSignal Transduction
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Inhibition of Rac1 signaling by lovastatin protects against anthracycline-induced cardiac toxicity

2011

Normal tissue damage limits the efficacy of anticancer therapy. For anthracyclines, the clinically most relevant adverse effect is cardiotoxicity. The mechanisms involved are poorly understood and putative cardioprotectants are controversially discussed. Here, we show that the lipid-lowering drug lovastatin protects rat H9c2 cardiomyoblasts from doxorubicin in vitro. Protection by lovastatin is related to inhibition of the Ras-homologous GTPase Rac1. It rests on a reduced formation of DNA double-strand breaks, resulting from the inhibition of topoisomerase II by doxorubicin. Doxorubicin transport and reactive oxygen species are not involved. Protection by lovastatin was confirmed in vivo. I…

rac1 GTP-Binding ProteinCancer ResearchAnthracyclineDoxorubicin transportCardiac fibrosismedicine.medical_treatmentImmunologyPharmacologyBiologyDNA damage responsestatinsMiceCellular and Molecular NeuroscienceRho GTPasespolycyclic compoundsmedicineAnimalsDNA Breaks Double-StrandedMyocytes CardiacDoxorubicinLovastatinanthracyclinesCardiotoxicityAntibiotics AntineoplasticTroponin IConnective Tissue Growth FactorCell Biologymedicine.diseaseRatsCTGFDNA Topoisomerases Type IICytokinenormal tissue damageDoxorubicinOriginal Articlelipids (amino acids peptides and proteins)LovastatinAtrial Natriuretic FactorSignal Transductionmedicine.drugCell Death & Disease
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