Search results for "mito"

showing 10 items of 2513 documents

Differential responses to docosahexaenoic acid in primary and immortalized cardiac cells

2013

Abstract The importance of dietary polyunsaturated fatty acids (PUFAs) in the reduction of cardiovascular disease has been recognized for many years. Docosahexaenoic acid (22:6n3, DHA) is an n-3 PUFA known to affect numerous biological functions and provide cardioprotection; however, the exact molecular and cellular protective mechanism(s) remain unknown. In contrast, DHA also possesses many anti-tumorgenic properties including suppressing cell growth and inducing apoptosis. In the present study, we investigated the effect of DHA toward H9c2 cells (an immortalized cardiac cell line) and neonatal primary cardiomyocytes (NCM). Cells were treated with 0 μM, 10 μM or 100 μM DHA for upto 48 h. C…

CardioprotectionDocosahexaenoic AcidsbiologyCaspase 3Cell SurvivalInterleukin-6Cell growthCytochrome cBlotting WesternCytochromes cGeneral MedicineMitochondrionToxicologyMitochondria HeartCell LineRatsCell biologyDocosahexaenoic acidApoptosiscardiovascular systembiology.proteinAnimalsMyocytes CardiacViability assayCaspaseToxicology Letters
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May the force be with you: Transfer of healthy mitochondria from stem cells to stroke cells

2018

Stroke is a major cause of death and disability in the United States and around the world with limited therapeutic option. Here, we discuss the critical role of mitochondria in stem cell-mediated rescue of stroke brain by highlighting the concept that deleting the mitochondria from stem cells abolishes the cells’ regenerative potency. The application of innovative approaches entailing generation of mitochondria-voided stem cells as well as pharmacological inhibition of mitochondrial function may elucidate the mechanism underlying transfer of healthy mitochondria to ischemic cells, thereby providing key insights in the pathology and treatment of stroke and other brain disorders plagued with…

Cardiorespiratory Medicine and HaematologyMitochondrionRegenerative medicineRats Sprague-Dawley0302 clinical medicineStem Cell Research - Nonembryonic - Humanenergy metabolismStrokeStem CellsBrainCerebral ischemiaMitochondriaStrokeNeurologycellular bioenergeticStem Cell Research - Nonembryonic - Non-HumanStem cellmedicine.symptomCardiology and Cardiovascular Medicine1.1 Normal biological development and functioningClinical SciencesEnergy metabolismregenerative medicineInflammation03 medical and health sciencesUnderpinning researchmedicineAnimalsHumansNeurology & NeurosurgeryAnimalbusiness.industryMechanism (biology)NeurosciencesStem Cell Researchmedicine.diseaseRatsBrain DisordersTransplantationDisease Models AnimalinflammationDisease ModelsCommentarycellular bioenergeticsSprague-DawleyNeurology (clinical)businessNeuroscience030217 neurology & neurosurgerytransplantationJournal of Cerebral Blood Flow & Metabolism
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From molecular mechanisms to clinical management of antineoplastic drug-induced cardiovascular toxicity: A translational overview

2019

Significance: Antineoplastic therapies have significantly improved the prognosis of oncology patients. However, these treatments can bring to a higher incidence of side-effects, including the worrying cardiovascular toxicity (CTX). Recent Advances: Substantial evidence indicates multiple mechanisms of CTX, with redox mechanisms playing a key role. Recent data singled out mitochondria as key targets for antineoplastic drug-induced CTX; understanding the underlying mechanisms is, therefore, crucial for effective cardioprotection, without compromising the efficacy of anti-cancer treatments. Critical Issues: CTX can occur within a few days or many years after treatment. Type I CTX is associated…

Cardiovascular toxicityPhysiologymedicine.medical_treatmentAntineoplastic drugClinical BiochemistryAntineoplastic Agents030204 cardiovascular system & hematologyPharmacologyBiochemistryCardiac cellcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factor; Antineoplastic Agents; Cardiotoxicity; Humans; Mitochondria; Oxidation-Reduction03 medical and health scienceschemistry.chemical_compoundErbB2 inhibitors cancer immunotherapy chemotherapy oxidative/nitrosative stress tyrosine kinase inhibitors vascular endothelial growth factor0302 clinical medicinetyrosine kinase inhibitorcancer immunotherapy; chemotherapy; ErbB2 inhibitors; oxidative/nitrosative stress; tyrosine kinase inhibitors; vascular endothelial growth factorChemotherapy; ErbB2 inhibitors; vascular endothelial growth factor; tyrosine kinase inhibitors; oxidative/nitrosative stress; cancer immunotherapyCancer immunotherapytyrosine kinase inhibitorsmedicineHumansChemotherapyMolecular BiologyGeneral Environmental ScienceCardioprotectionComprehensive Invited ReviewsChemotherapyErbB2 inhibitorcancer immunotherapyvascular endothelial growth factorbusiness.industryCell BiologyCardiotoxicityMitochondriaVascular endothelial growth factoroxidative/nitrosative streErbB2 inhibitorschemistry030220 oncology & carcinogenesisGeneral Earth and Planetary SciencesbusinessOxidation-ReductionAfter treatmentoxidative/nitrosative stress
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Transcriptional and post-transcriptional regulation of iNOS expression in human chondrocytes

2009

Chondrocytes are important for the development and maintenance of articular cartilage. However, both in osteoarthritis (OA) and rheumatoid arthritis (RA) chondrocytes are involved in the process of cartilage degradation and synthesize important immunomodulatory mediators, including nitric oxide (NO) generated by the inducible NO synthase (iNOS). To uncover the role of iNOS in the pathomechanisms of OA and RA, we analyzed the regulation of iNOS expression using immortalized human chondrocytes as a reproducible model. In C-28/I2 chondrocytes, iNOS expression was associated with the expression of the chondrocyte phenotype. Peak induction by a cytokine cocktail occurred between 6 and 8h and dec…

Cartilage Articularmedicine.medical_specialtyAnti-Inflammatory AgentsNitric Oxide Synthase Type IIBiologyBiochemistryp38 Mitogen-Activated Protein KinasesChondrocyteArticleGene Expression Regulation EnzymologicGlucocorticoid receptorChondrocytesReceptors GlucocorticoidInternal medicineGene expressionmedicineHumansRNA MessengerRNA Processing Post-TranscriptionalPost-transcriptional regulationCell Line TransformedPharmacologyRegulation of gene expressionNF-kappa B p50 SubunitRNA-Binding ProteinsInterferon-Stimulated Gene Factor 3Janus Kinase 2Cell biologyNitric oxide synthaseEndocrinologymedicine.anatomical_structureCell cultureEnzyme Inductionbiology.proteinTrans-ActivatorsCytokinesZearalenoneSignal transduction
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Cigarette Smoke Extract Induces p38 MAPK-Initiated, Fas-Mediated Eryptosis

2022

Eryptosis is a physiological mechanism for the clearance of senescent or damaged erythrocytes by phagocytes. Excessive eryptosis is stimulated under several pathologies and associated with endothelial injury and thrombosis. Cigarette smoke (CS) is an established risk factor for vascular diseases and cigarette smokers have high-levels of eryptotic erythrocytes. This study, for the first time, investigates the mechanism by which CS damages red blood cells (RBCs). CS extract (CSE) from commercial cigarettes was prepared and standardized for nicotine content. Cytofluorimetric analysis demonstrated that treatment of human RBCs with CSE caused dose-dependent, phosphatidylserine externalization an…

Caspase 8ErythrocytesCaspase 3cigarette smokeOrganic ChemistryGeneral Medicinep38 MAPKCeramidesp38 Mitogen-Activated Protein KinasesCatalysisComputer Science ApplicationsInorganic Chemistryeryptosis; cigarette smoke; death-inducing signaling complex (DISC); p38 MAPK; ceramide; caspasescaspasesSmokeeryptosisSettore BIO/10 - BiochimicaTobaccodeath-inducing signaling complex (DISC)HumansceramidePhysical and Theoretical ChemistryReactive Oxygen SpeciesMolecular BiologySpectroscopy
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Spatial regulation of the Start repressor Whi5

2009

The Saccharomyces cerevisiae Start repressor Whi5, the functional analogue of mammalian pRB, shuttles between the nucleus and the cytoplasm throughout the cell cycle: enters into the nucleus at the end of mitosis and remains nuclear until Start. We studied the mechanisms involved in this spatial regulation. The nuclear import depends on the beta-karyopherins of the classical import pathway Kap95 and Cse1. Whi5 contains a monopartite and a bipartite classical NLS localized in its N-terminal region which are functionally redundant. A fragment of Whi5 containing these NLSs is able to constitutively accumulate a GFP(4) protein inside the nucleus throughout the cell cycle, which suggests that th…

Cdc14Cell BiologyBiologyCell biologyCell nucleusmedicine.anatomical_structureBiochemistryCytoplasmmedicineNuclear transportNuclear proteinNuclear export signalCell Cycle ProteinMolecular BiologyMitosisDevelopmental BiologyCell Cycle
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Mitogenic effects of phospholipase D and phosphatidic acid in transiently permeabilized astrocytes: effects of ethanol.

2003

Investigations of lipid-mediated signalling pathways are often limited by a lack of methods for the intracellular delivery of lipid messengers. We established a procedure for the transient permeabilization of astrocytes by an oxygen-insensitive mutant of streptolysin-O (SLO) to investigate the participation of the phospholipase D (PLD) signalling pathway in astroglial cell proliferation. Exogenous PLD, when incubated in the presence of SLO, caused an increase in DNA synthesis (measured by thymidine incorporation) which was completely suppressed by ethanol (0.3%, v/v). In parallel experiments, phosphatidic acid also induced a dose-dependent mitogenic response which, however, was not affected…

Cell Membrane PermeabilityIndolesmedicine.drug_classPhosphatidic AcidsBiologyBiochemistryDiglyceridesCellular and Molecular Neurosciencechemistry.chemical_compoundBacterial ProteinsmedicinePhospholipase DAnimalsEnzyme InhibitorsProtein kinase ACells CulturedDiacylglycerol kinaseDNA synthesisDose-Response Relationship DrugEthanolPhospholipase DPhosphatidic acidDNAProtein kinase inhibitorRatschemistryBiochemistryAstrocytesStreptolysinslipids (amino acids peptides and proteins)Signal transductionMitogensIntracellularCell DivisionSignal TransductionJournal of neurochemistry
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Survivin’s Dual Role: An Export’s View

2007

Survivin is proposed to function as a mitotic regulator and an apoptosis inhibitor during development and pathogenesis. As such, survivin has aroused keen interest in disparate areas of basic and translational research. Survivin acts as a subunit of the chromosomal passenger complex (CPC), composed of the mitotic kinase Aurora-B, Borealin and INCENP, and is essential for proper chromosome segregation and cytokinesis. Our recent findings indicate that the nuclear export receptor Crm1 is critically involved in tethering the CPC to the centromere by interacting with a leucine-rich nuclear export signal (NES), evolutionary conserved in all mammalian survivin proteins. In addition, the survivin/…

Cell NucleusApoptosis InhibitorINCENPSurvivinActive Transport Cell NucleusCell BiologyCell cycleBiologyInhibitor of Apoptosis ProteinsNeoplasm ProteinsCell biologySurvivinAnimalsHumansNuclear export signalMicrotubule-Associated ProteinsneoplasmsMolecular BiologyMitosisCytokinesisNuclear localization sequenceDevelopmental BiologyCell Cycle
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Binucleate cells in the Ehrlich ascites tumor. Action of 5-fluorouracil.

1987

Time-dependent frequency distribution of binucleate cells (BC) was studied in Ehrlich ascites tumor (EAT) growing in mice. In animals that received no further treatment, the number of BC increased slowly from 2.6% to 16.5% of total cells within 8 days. In animals that were treated with different doses of 5-fluorouracil (FU) we found clearly higher numbers of BC. The number of BC increased with tumor age. The increase observed after treatment was reached more quickly in animals that had received the highest FU dose. The final number of BC was also dependent on the age of the tumor at the time of FU injection.

Cell NucleusDose-Response Relationship DrugCell BiologyGeneral MedicineBiologyPharmacologyEhrlich ascitesMiceFluorouracilImmunologymedicineMitotic IndexDistribution (pharmacology)AnimalsFemaleFluorouracilCarcinoma Ehrlich TumorAfter treatmentmedicine.drugBiology of the cell
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The autoantigen La/SSB: detection on and uptake by mitotic cells.

1992

Abstract The nuclear autoantigen La, a transcription/termination factor of RNA polymerase III, was recently shown to translocalize to the cell surface of growth-stimulated cells during transition from G0- to G1-phase. Here we describe the staining of living mitotic cells with the anti-La mab La11G7. Moreover, La protein added to cell culture medium was able to enter into synchronized mitotic cells. Uptake was inhibited by the anti-La mab. La protein taken up into prophase cells assembled into a fibrillar network. Taken up by ana/telophase cells, La protein was preferentially transported into the newly forming or formed nuclei. This import allowed us to study directly the intranuclear locali…

Cell NucleusNucleoplasmNucleolusCell MembraneAntibodies MonoclonalG0 phaseCell BiologyBiologyMolecular biologyAutoantigensProphaseAntibodiesCell LineCell nucleusmedicine.anatomical_structureRibonucleoproteinsCell culturemedicineTelophaseNuclear proteinTelophaseAnaphaseMitosisExperimental cell research
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