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ApoptosisInhibitor of Apoptosis ProteinsIn Situ Nick-End LabelingCaspase 3Myocardial Reperfusion InjuryCaspasesbcl-2-Associated X ProteinMyocardiumGene Expression ProfilingProto-Oncogene Proteins c-bcl-2NecrosisMyocytes, CardiacDNA FragmentationOligonucleotide Array Sequence AnalysisIschemic PostconditioningGene ExpressionTumor Necrosis Factor-alphaApoptosis Regulatory ProteinsSignal TransductionBlotting, WesternMyocardial IschemiaMyocardial InfarctionCells, CulturedRats, WistarCardiotonic AgentsDisease Models, AnimalCell Line, TumorX-Linked Inhibitor of Apoptosis ProteinMitochondria, HeartCell SurvivalApoptosis Inducing FactorCASP8 and FADD-Like Apoptosis Regulating ProteinRats, Sprague-DawleyCardiomyopathiesMice, Inbred C57BLImmunohistochemistryVentricular RemodelingCaspase InhibitorsCaspase 9Caspase 8MitochondriaFas Ligand ProteinEnzyme ActivationTumor Cells, CulturedTumor Suppressor Protein p53Receptors, Tumor Necrosis FactorCytochromes cHeartbcl-X ProteinCell LineAnnexin A5Cell ProliferationFlow CytometryAmino Acid Chloromethyl KetonesCysteine Proteinase InhibitorsTNF-Related Apoptosis-Inducing LigandProto-Oncogene ProteinsAntineoplastic AgentsCell CyclePoly(ADP-ribose) PolymerasesEnzyme InhibitorsReactive Oxygen SpeciesTransfectionNF-kappa BJurkat CellsCell DivisionDose-Response Relationship, DrugRNA, MessengerCell DeathDown-RegulationRNA, Small InterferingMembrane GlycoproteinsCaspase 7HL-60 CellsTime FactorsMembrane Potential, MitochondrialUp-RegulationPhosphorylationGenes, bcl-2Reverse Transcriptase Polymerase Chain Reactionbcl-2 Homologous Antagonist-Killer ProteinCytochrome c GroupBH3 Interacting Domain Death Agonist ProteinProto-Oncogene Proteins c-aktMyeloid Cell Leukemia Sequence 1 ProteinDNA DamageMice, KnockoutReceptors, TNF-Related Apoptosis-Inducing LigandGene Expression RegulationStaurosporineDrug SynergismCarrier ProteinsGene Expression Regulation, NeoplasticCeramidesReceptors, Tumor Necrosis Factor, Type IIOxidative StressProtein-Serine-Threonine Kinasesbcl-Associated Death ProteinHeLa CellsFas-Associated Death Domain Protein
InfarctionCardiomyocytesAcuteCytokinesDysfunctionCardiomyocyte apoptosisStunned myocardiumIschemicAutophagyProliferationLeft ventricularProteinAngiogenesisCause apoptosisInflammationHypoxia-inducedMacrophage infiltrationMechanisticallyContractilityTarget genesIschemia and reperfusionApoptoticHypertrophyInhibitionEndothelialPathwaysMAPKProteinsInfarct sizeCardiovascularReoxygenationCoronary blood flowRegulateAtrialTumourInfiltrationLipid peroxidationReperfusion injuryMechanismsAtherosclerosisMitochondrialTissueAlterationsRatsOcclusionDifferentiationPathogenInflammatory responseExpressionDecreasesPathogenesisMetabolismAssayCell deathFunctional
Infarction22
Cardiomyocytes8
  • Delivery of miRNA-210 to an ischemic heart improves heart function, possibly by promoting the release of angiogenic factors like interleukin-1α (IL-1α), tumor necrosis factor-α (TNF-α) and leptin, as seen in HL-1 cardiomyocytes injected with miRNA-210. (wikipedia.org)
  • Therefore, suppression of these two particular genes may contribute to the improvement of cardiac tissue and function by up-regulating angiogenesis and inhibiting apoptosis of cardiomyocytes after myocardial infarct. (wikipedia.org)
  • Res effectively suppress the cardiomyocytes hypertrophy and apoptosis induced by ISO, characterized by the reduction of the myocardial cell surface area, the ANP gene expression, the LDH and MDA leakage amount and the rate of cell apoptosis, while decrease of the protein expression of GRP78, GRP94 and CHOP, and reverse the expression of Bcl-2 and Bax. (karger.com)
  • Apoptosis of cardiomyocytes was evaluated by TUNEL assay and flow cytometry analysis. (ehu.eus)
  • Furthermore, administration of EGCG in vitro was observed to prevent apoptosis of cardiomyocytes by regulating pro-apoptotic and anti-apoptotic proteins, including B cell lymphoma-2 (Bcl-2) and Bcl-2-associated X protein, and by simultaneously regulating caspase-3 in isolated rat hearts ( 13 ). (spandidos-publications.com)
  • Activated TNF and the FasFas ligand program play a important function within the apoptosis of cardiomyocytes [39] and this may perhaps ADAM17 Inhibitor Source explain high Fas-L levels in diabetic sufferers. (amparinhibitor.com)
  • There is a growing body of evidence which demonstrates that following ACS, microRNAs might inhibit fibroblast proliferation and scarring, as well as harmful apoptosis of cardiomyocytes, and stimulate fibroblast reprogramming into induced cardiac progenitor cells. (archivesofmedicalscience.com)
  • The characteristics of heart failure involve progressive left ventricular dysfunction and loss of cardiomyocytes via necrosis or apoptosis [55]. (city-made.com)
Acute3
  • Our study found that fibrinogen-like protein 2 (Fgl2) gene silencing activates angiopoietin/Tie system and induces myocardial microvascular endothelial Cells proliferation and cell migration, we also found that serum Fgl2 levels elevated in patients with acute coronary syndrome (ACS), these results are preliminary, but very meaningful [ 1 , 2 ]. (silverchair.com)
  • Stunned myocardium is myocardium that suffers transient reversible myocardial contractile dysfunction that is caused by acute ischemia during which the blood supply is almost completely restored by reperfusion, with no metabolic deterioration. (medscape.com)
  • Acute MI may be either of the nonreperfusion type, in which case the obstruction to blood flow is permanent, or of the reperfusion type, in which the obstruction or lack of blood flow is long enough in duration (generally hours) but is reversed or restored after myocardial cell death occurs. (medscape.com)
Cytokines7
  • Furthermore, the hibernator cardioprotective phenotype is also associated with reduced myocardial NF-κB activity, reduced expression of downstream cytokines and neutrophil extravasation following cardiac surgery. (duke.edu)
  • The endotoxin-induced myocardial dysfunction probably depends on the toll-like receptor (TLR) 4-induced cytokines release as a delay in onset of myocardial depression after endotoxin administration ( 10 ). (frontiersin.org)
  • Treatment with olmesartan attenuated the myocardial mRNA expressions of proinflammatory cytokines, [Interleukin (IL)-1β, monocyte chemoattractant protein-1, tumor necrosis factor-α and interferon-γ)] and the protein expression of tumor necrosis factor-α compared with that of vehicle-treated rats. (ijbs.com)
  • This inflammatory response has been further identified in damaged myocardium during propagation of chronic HF to promote monocyte activation and the further production of cytokines, thus augmenting cardiac dysfunction [23], resulting in myocardial fibrosis and cardiac remodeling [24]. (researchsquare.com)
  • Hyperglycemia and oxidative pressure activate NF-B, which regulates the expression of big numbers of genes such as pro-inflammatory cytokines (TNF- and IL-1) and numerous genes correlated to fibrosis, like TGF-, inside the diabetic heart [7, 36]. (amparinhibitor.com)
  • The aim of this research was to study polymorphisms in the genes encoding cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in patients with celiac disease (CD) antigens DQ2 (DQ2-positive) or DQ8 (DQ8-positive). (geneticsmr.com)
  • Here we investigated roles for miR-126 in stress kinase activation, induction of inflammatory cytokines and apoptosis caused by exposure of cultured cardiac myocytes to hypoxia/acidosis or acidosis alone. (biomedres.us)
Dysfunction7
  • Mechanisms for myocardial cell dysfunction, death (apoptosis/necrosis) and autophagy. (nih.gov)
  • The term hibernating myocardium is also used to indicate chronic myocardial contractile dysfunction due to ischemia, in which there is reduced coronary blood flow at rest and increased myocardial demand results in impaired contractility. (medscape.com)
  • Finding all 3 entities in the same patient with chronic myocardial dysfunction is not uncommon (see the image above). (medscape.com)
  • Other TLR-related genes (TLR2, 3, and 9) were demonstrated to be involved in sepsis-induced cardiac dysfunction from recent studies. (frontiersin.org)
  • However, questions remain as to whether apoptosis is a critical event in the transition from compensated to decompensated cardiac hypertrophy and the onset of ventricular dysfunction. (latestfashiontips.com)
  • Additionally, it may clinically manifest with myocardial necrosis, cardiac arrhythmia, myocardial stunning and microvascular dysfunction ( 5 ). (spandidos-publications.com)
  • However, myocardial ischemia-reperfusion (I/R) can aggravate ischemia-induced cardiac dysfunction and myocardial cell damage, leading to intracellular calcium overload, apoptosis, and inflammation. (geneticsmr.com)
Cardiomyocyte apoptosis3
  • MiRNA-210 in particular, has been studied for its effects in rescuing cardiac function after myocardial infarcts via the up-regulation of angiogenesis and inhibition of cardiomyocyte apoptosis. (wikipedia.org)
  • The aim of this study was to investigate whether resveratrol (RSV) could ameliorate ischemia- and hypoxia-associated cardiomyocyte apoptosis and injury via inhibiting senescence signaling and inflammasome activation. (hindawi.com)
  • What is the pathophysiologic significance of cardiomyocyte apoptosis in heart failure? (latestfashiontips.com)
Stunned myocardium1
  • Clinically, discerning the etiology of depressed myocardial contractile function is difficult, whether due to stunned myocardium, silent ischemia, or hibernating myocardium. (medscape.com)
Ischemic6
  • HNE mediates necrosis, apoptosis, and autophagy within the area rendered ischemic over the first 6 to 24 hours. (lsuhs.edu)
  • Compared to rats, AGS display robust myocardial ischemic tolerance following DHCA (both reduced myocardial necrosis and apoptosis). (duke.edu)
  • [ 1 ] Therefore, an area of necrosis or scarring is considered to have an "ischemic pattern" if it is largest at the endocardium, with a wedge-shaped extension up to the epicardial surface. (medscape.com)
  • Numerous studies have evaluated the association between the -174 G/C polymorphism in the interleukin-6 ( IL6 ) gene and ischemic stroke risk. (geneticsmr.com)
  • Cardiac myocyte cell death by apoptosis accompanies heart disease of both ischemic and nonischemic origin [1-3]. (biomedres.us)
  • Inhibition of Na+/H+ exchange is protective against ischemic injury, while inhibition of the vacuolar ATPase promotes apoptosis, in part by shifting the proton load toward the Na+/H+ transporter and thus increasing Ca2+ uptake, and in part by reducing the myocyte capacity to control [pH]i. (biomedres.us)
Autophagy4
Proliferation2
  • The effect of antioxidant trolox on biological characteristics of MSCS, including aging, proliferation, and gene expression, was examined. (techscience.com)
  • Experimentally confirmed target genes were identified for the 73 diagnostic miRNAs, from which proliferation genes were selected from CRISPR-Cas9/RNA interference (RNAi) screening assays. (cdc.gov)
Left ventricular2
  • The concomitant presence of myocardial necrosis with myocardial ischemia, stunning, or hibernation may complicate appraisal of left ventricular (LV) function and patient management. (medscape.com)
  • Cardiac transcriptome sequencing on left ventricular myocardial samples found 29,740 genes expressed and 1267 differentially expressed genes. (auburn.edu)
Protein11
  • In contrast to protein interaction networks, enriched gene ontology (GO) terms of AMI related genes were used to construct a gene ontology interaction (GOI) network, which can be used to simulate the functional interactions between differential expressed genes of disease. (frontiersin.org)
  • The second target gene, protein tyrosine phosphatase-1B (Ptp1b) is involved in the induction of apoptosis. (wikipedia.org)
  • Ptp1b gene protein has been known to regulate apoptosis by regulating the phosphorylation status of apoptotic proteins such as caspase-3 and caspase-8. (wikipedia.org)
  • Protein expression of ER stress and apoptosis factors was analyzed using Western Blot analysis. (karger.com)
  • Fibrinogen-like protein 2 (Fgl2) is involved in apoptosis, angiogenesis and inflammatory response. (silverchair.com)
  • We found that Fgl2 gene silencing inhibits apoptosis and improves heart function of streptozotocin (STZ)-induced diabetes rats, the possible mechanism maybe that Fgl2 gene silencing reduces the tumour necrosis factor (TNF)±levels, decreases the expression of B-cell lymphoma-2 (bcl2), bcl-2-associated X (bax), toll-like receptors 4 (TLR4) and p38 mitogen-activated protein kinase (MAPK). (silverchair.com)
  • Several lines of evidence suggest that apoptosis-inducing factor mitochondrion-associated protein (AIFm2), a p53 target gene, a redox-responsive protein that resides in mitochondria and plays a central role in the caspase-independent cell death pathway. (lsuhs.edu)
  • Myocardial protein expressions of AT 1 R, NADPH oxidase subunits (p47phox, p67phox, gp91phox) and the expression of markers of oxidative stress (3-nitrotyrosine and 4-hydroxy-2-nonenal), and the cardiac apoptosis were also significantly decreased by the treatment with olmesartan compared with those of vehicle-treated rats. (ijbs.com)
  • Furthermore, olmesartan treatment down-regulated the myocardial expressions of glucose regulated protein-78, growth arrest and DNA damage-inducible gene, caspase-12, phospho-p38 mitogen-activated protein kinase (MAPK) and phospho-JNK. (ijbs.com)
  • Binding insulin to the insulin receptor recruits PI3K to the plasma membrane which then activates the central mediator of insulin's effects, Akt-1 also called protein kinase B. Protein kinase B inhibits apoptosis, stimulates myocyte hypertrophy/fibrosis, and nitric oxide (NO) production. (thepmc.org)
  • Pansensitive and panresistant genes to 21 NCCN-recommended drugs with concordant mRNA and protein expression were identified. (cdc.gov)
Angiogenesis3
  • However, miRNA-210 also targets the Efna3 and Ptp1b genes, which are genes which endogenously regulate angiogenesis and apoptosis, respectively. (wikipedia.org)
  • Ephrin-A3 (Efna3) is a gene that is involved in the inhibition of angiogenesis. (wikipedia.org)
  • Diabetes is closely associated with apoptosis, angiogenesis and coagulation. (silverchair.com)
Cause apoptosis2
Inflammation3
  • Skeletal muscle pathology in affected dogs is similar to what has been described in people with DMD and includes myocyte degeneration, necrosis, and regeneration, fibrofatty infiltration, lymphohistiocytic inflammation, and mineralization. (auburn.edu)
  • The potential association of SUG-induced alteration in cholesterol homeostasis with oxidative stress and apoptosis activation buy cheap prednisone online the fact that resistance/sensitivity to oxidative stress may likely differ between brain regions and neuronal cell types, potential neurons-astrocytes interactions, as well as modulation by pathological mechanisms such as inflammation, all represent new research windows that deserve further studies. (city-made.com)
  • Key apoptotic pathway intermediates and inflammation markers IL-6, IL-8, and tumor necrosis factor (TNF) were quantified by western blot analyses, while miR-126 expression was tracked by quantitative polymerase chain reaction (qPCR). (biomedres.us)
Hypoxia-induced3
  • In in vitro experiment, RSV prevented hypoxia-induced NRCM senescence and apoptosis. (hindawi.com)
  • The p53-associated signaling pathway has been demonstrated to regulate hypoxia-induced apoptosis and senescence [ 5 ]. (hindawi.com)
  • Here, we investigated the role of circ-JA760602 in modulating the apoptosis of hypoxia-induced AMI cells using the AC16 cardiomyocyte in vitro cell model. (ehu.eus)
Macrophage infiltration1
  • Consequently, a greater post-MI monocyte-derived myocardial macrophage infiltration was noted in Hmox1-deficient individuals. (springer.com)
Mechanistically1
  • Mechanistically this is accompanied by preservation of myocardial PPARα activity in AGS, which is significantly downregulated in the rat, and a metabolic phenotype consistent with the development of mitochondrial substrate flux "bottlenecks" in rats (myocardial accumulation of acylcarnitines and ceramides, organic acid profiles consistent with compromised citric acid cycle flux) compared to AGS. (duke.edu)
Contractility4
  • Through the network analysis, reduction of cardiac preload and myocardial contractility was shown to be the major effect of Schisandra components, which was further experimentally validated. (frontiersin.org)
  • In addition, the expression of NCOR2 and NFAT in myocyte were experimentally confirmed to be associated with Schisandra in the treatment of AMI, which may be responsible for the preservation effect of myocardial contractility. (frontiersin.org)
  • The majority of the above-mentioned genes have known roles in cardiac compensatory changes secondary to dystrophinopathic-associated damage, including survival, remodeling, contractility, conduction, and immunoregulation. (auburn.edu)
  • Differential expression of genes was also observed in pathways associated with cardiac oxidative stress, apoptosis, and contractility. (auburn.edu)
Target genes2
  • Using a clinically relevant model of surgical deep hypothermic circulatory arrest (DHCA) combined with targeted metabolomic and proteomic profiling, we are investigating how changes in hibernation-specific myocardial expression/activity of PPARα nuclear receptor and downstream target genes (FGF21) following cardiac surgery can provide cardioprotection by increasing myocardial fatty acid oxidation and inhibiting NF-κB regulated pro-inflammatory responses. (duke.edu)
  • MicroRNAs are small non-coding post-translational biomolecules which, when expressed, modify their target genes. (archivesofmedicalscience.com)
Ischemia and reperfusion2
  • In contrast, concentric subendocardial necrosis may result from global ischemia and reperfusion in cases of prolonged cardiac arrest with resuscitation. (medscape.com)
  • In animal models, increased apoptosis accompanies both phases of ischemia and reperfusion [8]. (biomedres.us)
Apoptotic5
  • During apoptosis, apoptotic bodies are formed within cells. (hindawi.com)
  • The morphologic changes seen in apoptosis include cell shrinkage, loss of cell-cell contacts, membrane blebbing, and nuclear condensation, terminating in the breakdown of the cell into apoptotic bodies that are phagocytosed by surrounding cells. (latestfashiontips.com)
  • Activation of the mitochondrial apoptotic process is regarded as the point of no return in apoptosis. (latestfashiontips.com)
  • Heart failure is characterized by a significant increase in apoptotic myocyte death in spite of the enhanced expression of antiapoptotic gene products in the cells. (latestfashiontips.com)
  • Apoptosis, on the other hand, is characterized by cell shrinkage, membrane blebbing, condensation, margination of nuclear chromatin, packaging of apoptotic bodies, and engulfment of the immunogenic intracellular proteins by phagocytes and macrophages. (bioradiations.com)
Hypertrophy2
  • Hypertrophy was estimated by measuring the cell surface area and the atrial natriuretic peptide (ANP) gene expression. (karger.com)
  • In summary, Res treatment effectively suppressed myocardial hypertrophy and apoptosis at least partially via inhibiting ER stress. (karger.com)
Inhibition1
Endothelial4
  • In this study, we profiled the gene expression of human umbilical vein endothelial cells (HUVECs) exposed to different concentrations of TCDD by high-throughput sequencing. (elsevierpure.com)
  • Cell survival during ischemia/reperfusion is governed by HIF-1α-dependent genes such as heme oxygenase-1, inducible nitric oxide synthase, cyclooxygnease-2, and vascular endothelial growth factor. (springeropen.com)
  • Studies of human umbilical vein endothelial cells (HUVEC) and arterial endothelial cells (HAEC) showed that therapeutically relevant concentrations of MTX phosphorylate AMPKα Thr172 , and induce cytoprotective genes including manganese superoxide dismutase (MnSOD) and haem oxygenase-1 (HO-1). (bmj.com)
  • Furthermore, MTX protected against glucose deprivation-induced endothelial apoptosis. (bmj.com)
Pathways3
  • These findings are significant because they support the use of the Australian Labradoodle as a novel animal model for the study of DMD cardiomyopathy, they elucidate pathways and differential gene expression involved in Labradoodle dystrophinopathic cardiomyopathy, and they may aid in the development of therapeutic targets to treat dystrophinopathy-associated cardiac disease. (auburn.edu)
  • KEGG pathway analysis showed that many genes in the signaling pathways of vascular smooth muscle contraction and apoptosis were altered distinctly. (elsevierpure.com)
  • In addition, FN has been shown to inhibit apoptosis via various intracellular pathways 20 . (nature.com)
MAPK2
Proteins3
  • Cellular mechanisms of arrhythmogenesis: genes and proteins involved. (nih.gov)
  • Unlike necrosis, an unregulated form of cell death caused by external physicochemical stress, necroptosis is highly regulated and acts as a defense mechanism or escape route for cells infected with viruses that inhibit apoptosis signaling proteins (examples of these viruses include the murine cytomegalovirus, West Nile virus, human immunodeficiency virus-1 (HIV-1), and herpes simplex virus). (bioradiations.com)
  • In contrast, inflammatory pathologies, such as multiple sclerosis, myocardial ischemia-reperfusion injury, inflammatory bowel disease, and chronic obstructive pulmonary disease, are associated with elevated expression of necroptotic signaling proteins. (bioradiations.com)
Infarct size1
  • MG53 KO mice lack IPC-mediated cardioprotection as evidenced by a failure of IPC to reduce IR-induced myocardial infarct size. (biomedcentral.com)
Cardiovascular1
  • However, the precise global gene expression alterations caused by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in the cardiovascular system need to be further elucidated. (elsevierpure.com)
Reoxygenation2
  • Increases in knowledge have revealed that the common pathophysiological scenario, myocardial ischemia reperfusion injury, including ischemia/reperfusion (I/R) and hypoxia/reoxygenation (H/R) forms of injury, results in depressed myocardial function and harmful morphological alterations, which may lead to heart failure ( 4 ). (spandidos-publications.com)
  • Rather, coincident acidosis and/or reoxygenation is required to trigger apoptosis [9-11]. (biomedres.us)
Coronary blood flow2
  • Rahimtoola suggested that hibernating myocardium is characterized by a state of persistently impaired myocardial and LV function at rest due to reduced coronary blood flow that can be partially or completely restored to normal by improving blood flow or by reducing oxygen demand (see the image below). (medscape.com)
  • Fast, effective recovery of the coronary blood flow, after myocardial ischemia, is an effective method to treat this ischemia. (geneticsmr.com)
Regulate2
  • MicroRNAs function to regulate the expression levels of other genes by several mechanisms. (wikipedia.org)
  • MicroRNAs regulate gene expression at the post-transcriptional level by binding to 3′- or less often to 5′-untranslated regions of target messenger RNAs (mRNAs), which in consequence leads to inhibited translation and/or induces degradation of targeted mRNA [ 1 ]. (archivesofmedicalscience.com)
Atrial1
Tumour1
  • These responses were preserved when HUVECs were pretreated with tumour necrosis factor-α to mimic dysfunctional endothelium. (bmj.com)
Infiltration1
  • Sparstolonin B was showed to alleviate joint swelling in RA rats, inhibited inflammatory cell infiltration and the release of ROS, reduced damage caused by oxidative stress, and suppressed the rate of apoptosis in synovial cells. (hindawi.com)
Lipid peroxidation2
Reperfusion injury3
  • The lack of effective treatments to reduce the consequences of myocardial ischemia-reperfusion injury and the increased reliance on percutaneous and surgical treatments for coronary and valvular disease or end-stage heart failure make it critically important to identify new targets and strategies for cardioprotection. (duke.edu)
  • oxidative stress that occurs during reperfusion injury has been shown to induce apoptosis, over and above that induced by ischemia. (latestfashiontips.com)
  • It has previously been demonstrated that phosphatidylinositol‑3‑kinase (PI3K)/Akt and cleaved caspase‑3 serve critical roles in the apoptosis of cardiac myocytes following ischemia/reperfusion injury. (spandidos-publications.com)
Mechanisms2
  • Our laboratory combines comparative biology approaches in multiple organisms with translational functional genomics to study the mechanisms underlying perioperative myocardial injury, with a particular emphasis on endogenous cardioprotective responses involving attenuation of nuclear factor-kappa B regulated inflammatory signaling and changes in myocardial fuel utilization. (duke.edu)
  • Epigenetic mechanisms are one of the essential regulators of gene expression which do not involve altering the primary nucleotide sequence. (ehu.eus)
Atherosclerosis2
  • Moreover, the transcripts of interleukin 1 beta (IL-1β) and tumor necrosis factor α (TNFα), which are related to atherosclerosis, were up-regulated by TCDD stimulation. (elsevierpure.com)
  • In this review, we focus on the role of cardiomyocyte-derived and cardiac fibroblast-derived microRNAs that are involved in the regulation of genes associated with cardiomyocyte and fibroblast function and in atherosclerosis-related cardiac ischemia. (archivesofmedicalscience.com)
Mitochondrial3
  • Impact of diet, obesity or systemic metabolic disorders on myocardial metabolism mitochondrial function, or the response to ischemia/reperfusion. (nih.gov)
  • Mitochondrial involvement in apoptosis is evidenced by the loss of the mitochondrial membrane, opening of mitochondrial transition pores, disruption of the electron transport chain, generation of reactive oxygen species, and translocation of cytochrome cto the cytoplasm, where it activates caspases. (latestfashiontips.com)
  • Countering NADH production, calcium action on the mitochondrial permeability transition pores increases inner membrane permeability thereby reducing proton potential, causing the matrix to swell and ultimately releasing cytochrome c (an initiator of apoptosis). (benbest.com)
Tissue1
  • Myocardial ischemia is a clinical syndrome manifesting a variety of tissue effects and global cardiac effects that impair cardiac function. (medscape.com)
Alterations1
Rats2
  • Myocardial functional parameters measured by hemodynamic and echocardiographic analyses were significantly improved by the treatment with olmesartan compared with those of vehicle-treated rats. (ijbs.com)
  • However, one month treatment of diabetic rats with troxerutin restored glucose and insulin levels, significantly decreased expression of inflammatory genes and pro-inflammatory mediators and increased microRNA level in comparison to diabetic group (p (kjpp.net)
Occlusion2
  • Regional myocardial function and electrophysiological alteration after coronary artery occlusion. (medscape.com)
  • Left main coronary artery occlusion generally results in a large anterolateral infarct, whereas occlusion of the left anterior descending coronary artery causes necrosis limited to the anterior wall. (medscape.com)
Differentiation2
  • In addition, Sox family genes colocalized with Runx2 and Lef1 , which are highly enriched in MSCs undergoing osteoblast differentiation. (ehu.eus)
  • Among them, Runx2 is a key target gene affecting osteogenic activity, and Cbfa1 regulates the differentiation of MSCs into osteoblasts at the transcriptional level. (cusabio.com)
Pathogen2
  • Researchers discovered that excessive induction of Fgl2 under certain medical conditions (e.g., pathogen invasion) could trigger complement activation, inflammatory response, cellular apoptosis and immune dysfunctions. (silverchair.com)
  • This second class of genes dissemble downstream of pathogen order voltaren 50mg binding to trigger the Dar response to infection. (centralparkcarriagesofficial.org)
Inflammatory response1
Expression14
  • Gene therapy and gene editing technology: Transcriptional and posttranscriptional regulation of gene expression. (nih.gov)
  • RSV also inhibited expression of interleukin- (IL-) 1 β , IL-6, tumor necrosis factor- α , and IL-18 in vivo . (hindawi.com)
  • Expression of 1,838 genes was changed significantly after TCDD stimulation. (elsevierpure.com)
  • We found that gene expression of β1-adrenoceptors (ADRB1), β2-adrenoceptors (ADRB2), endothelin-converting enzyme 1 (ECE1), and endothelin-1 gene (EDN1) that are involved in the blood pressure regulation pathway decreased apparently under TCDD treatment. (elsevierpure.com)
  • This leads to improper gene production (expression), which stimulates further neurohormonal hyperactivity leading to increasing cellular damage and death. (ceufast.com)
  • Following knockdown of Dnmt1 and Dnmt3a in zygotes, expression levels of Cdx2 in the trophectoderm and Nanog in the inner cell mass were measured, as well as p62 levels, reactive oxygen species (ROS) production, and apoptosis levels after 96 hours in embryo culture. (ehu.eus)
  • Using single-cell RNA-sequencing data, we examined the expression profiles of Sox genes in the mouse incisor dental pulp. (ehu.eus)
  • who reported that ALA decreased Fas-L gene expression in the hearts of diabetic animals and prevented the activation of death receptor signaling [41]. (amparinhibitor.com)
  • Moreover, DATS and CAP significantly up-regulated PI3K, Akt, and eNOS gene expression but down-regulated FOXO-1 expression compared to ISO group. (springeropen.com)
  • The downstream regulator of PI3K/Akt is hypoxia-inducible factor-1α (HIF-1α) which is a master regulator of gene expression in hypoxia, and it has the ability to influence cellular adaptive responses to hypoxia or ischemia. (springeropen.com)
  • The aim of this study was to investigate expression of tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in invasive pituitary adenomas (IPAs). (geneticsmr.com)
  • In addition, microRNAs (miRNAs), non-coding RNAs in the cell cytoplasm, have been known to be a regulator of gene expression through interaction with the complementary section of its target mRNAs, and play crucial physiological roles in cell function hemostasis as a suppressor or enhancer in gene expression. (kjpp.net)
  • MEK can phosphorylate and activate ERK, which is transferred into the nucleus and regulates gene expression by activating other kinases or transcription factors. (cusabio.com)
  • Significant downregulation of beta-defensin1 gene (DEFB1) expression was observed when human bronchial epithelial cells (HBEpCs) were exposed to IAV. (cdc.gov)
Decreases1
  • This concept of an adaptive process that shuts down the contractile process and decreases myocardial oxygen demand in the presence of chronically or intermittently reduced blood flow has generated considerable interest in clinical and experimental settings. (medscape.com)
Pathogenesis1
  • The considerable correlations of Fas-L and TNF- with e'a' ratio and ventricular worldwide peak systolic strain in diabetic sufferers may demonstrate that apoptosis plays a part in the pathogenesis of DCM. (amparinhibitor.com)
Metabolism2
  • Interestingly, this winter cardioprotective phenotype is associated not only with suppression of metabolic demand, but also with a fuel shift from myocardial carbohydrate to fatty acid (FA) metabolism. (duke.edu)
  • We feel that developing strategies to help 'switch' myocardial metabolism to resemble that naturally occurring in mammalian hibernators represents a transformative approach that could ultimately have an important positive impact in patients undergoing cardiac surgery and transplantation, as well as in victims of cardiac arrest, stroke, trauma and hypothermia, in addition to fundamentally advancing the field of nuclear receptor biology and myocardial substrate metabolism under extremes of physiology. (duke.edu)
Assay1
  • HBEpCs overexpressing DEFB1 caused a significant reduction in IAV, that was confirmed by IAV matrix gene analysis, plaque assay, and confocal microscopy. (cdc.gov)
Cell death5
Functional1
  • Our data show that a careful analysis of specific sites may reveal important and functional gene regulatory unfavourable weathers. (centralparkcarriagesofficial.org)