Search results for "FOXO1"

showing 6 items of 6 documents

Molecular adaptations of the blood–brain barrier promote stress resilience vs. depression

2020

Significance Thirty to fifty percent of depressed individuals are unresponsive to commonly prescribed antidepressant treatments, suggesting that biological mechanisms, such as stress-induced inflammation and blood vessel dysfunction, remain untreated. The blood–brain barrier is the ultimate frontier between the brain and harmful toxins or inflammatory signals circulating in the blood. Depression and vulnerability to chronic social stress are associated with loss of this barrier integrity; however, the mechanisms involved remain poorly understood. Identification of adaptations leading to resilience under stressful conditions could help develop novel treatments. Here we combined behavioral, p…

MaleHistone Deacetylase 1InflammationFOXO1Blood–brain barrierNucleus AccumbensEpigenesis GeneticProinflammatory cytokineMice03 medical and health sciences0302 clinical medicinevascularmedicineAnimalsHumansClaudin-5030304 developmental biologyInflammationSocial stressDepressive Disorder Major0303 health sciencesantidepressantMultidisciplinaryDepressionbusiness.industrySystems BiologyBiological Sciencesmedicine.diseasemood disordersAntidepressive Agents3. Good healthMice Inbred C57BLDisease Models Animalmedicine.anatomical_structureMood disordersBlood-Brain BarrierMajor depressive disorderAntidepressantmedicine.symptombusinessNeuroscienceStress Psychologicalepigenetic030217 neurology & neurosurgerySignal TransductionProceedings of the National Academy of Sciences
researchProduct

Altered REDD1, myostatin, and Akt/mTOR/FoxO/MAPK signaling in streptozotocin-induced diabetic muscle atrophy

2011

Type 1 diabetes, if poorly controlled, leads to skeletal muscle atrophy, decreasing the quality of life. We aimed to search highly responsive genes in diabetic muscle atrophy in a common diabetes model and to further characterize associated signaling pathways. Mice were killed 1, 3, or 5 wk after streptozotocin or control. Gene expression of calf muscles was analyzed using microarray and protein signaling with Western blotting. We identified translational repressor protein REDD1 (regulated in development and DNA damage responses) that increased seven- to eightfold and was associated with muscle atrophy in diabetes. The diabetes-induced increase in REDD1 was confirmed at the protein level. …

Malemedicine.medical_specialtyMAP Kinase Signaling SystemPhysiologyEndocrinology Diabetes and MetabolismFOXO1P70-S6 Kinase 1MyostatinBiologyMiceRandom Allocation03 medical and health sciences0302 clinical medicinePhysiology (medical)Internal medicinemedicineAnimalsRNA MessengerPhosphorylationMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathwayOligonucleotide Array Sequence Analysis030304 developmental biology0303 health sciencesForkhead Box Protein O1Gene Expression ProfilingTOR Serine-Threonine KinasesUbiquitinationForkhead Transcription FactorsOrgan SizeMyostatinProtein ubiquitinationMuscle atrophyMuscular AtrophyDNA Repair EnzymesDiabetes Mellitus Type 1EndocrinologyGene Expression Regulationbiology.proteinPhosphorylationmedicine.symptomProto-Oncogene Proteins c-akt030217 neurology & neurosurgeryTranscription FactorsAmerican Journal of Physiology-Endocrinology and Metabolism
researchProduct

Mboat7 down-regulation by hyper-insulinemia induces fat accumulation in hepatocytes.

2020

Background: Naturally occurring variation in Membrane-bound O-acyltransferase domain-containing 7 (MBOAT7), encoding for an enzyme involved in phosphatidylinositol acyl-chain remodelling, has been associated with fatty liver and hepatic disorders. Here, we examined the relationship between hepatic Mboat7 down-regulation and fat accumulation. Methods: Hepatic MBOAT7 expression was surveyed in 119 obese individuals and in experimental models. MBOAT7 was acutely silenced by antisense oligonucleotides in C57Bl/6 mice, and by CRISPR/Cas9 in HepG2 hepatocytes. Findings: In obese individuals, hepatic MBOAT7 mRNA decreased from normal liver to steatohepatitis, independently of diabetes, inflammatio…

Research paperTGFβ Transforming Growth Factor BetaIntracellular SpaceCRISPR Clustered Regularly Interspaced Short Palindromic RepeatshHEPS Human HepatocytesMice0302 clinical medicineLPIAT1DAG Diacylglyceroli.p. Intraperitonealmedia_commonFatty AcidsGeneral Medicine3. Good health030220 oncology & carcinogenesisHOMA-IR homeostasis Model Assessment of Insulin ResistanceMPO morpholinolcsh:Medicine (General)medicine.medical_specialtyPE Phosphatidyl-EthanolamineNashGeneral Biochemistry Genetics and Molecular Biology03 medical and health sciencesTNFα tumor Necrosis Factor AlphaLDL Low Density LipoproteinsHyperinsulinismNAFLDSD Standard Dietmedia_common.cataloged_instanceHumansCPT1 Carnitine Palmitoyltransferase IPhosphatidylinositolGene SilencingEuropean unionVLDL Very Low Density Lipoproteinlcsh:RhHSC Human Hepatic Stellate Cellsmedicine.diseaseLipid MetabolismOA Oleic AcidCI Confidence IntervalMboat7 Membrane bound O-acyltransferase domain containing 7MCD methionine choline deficient diet030104 developmental biologyEndocrinologychemistryCDP Cytidine-DiphosphateFOXO1 Forkhead Box protein O1NAFLD nonalcoholic fatty liver diseaseSteatohepatitisBMI Body Mass IndexCL CardiolipinAcyltransferases0301 basic medicineAlcoholic liver diseaseCXCL10 C-X-C Motif Chemokine 10lcsh:Medicinechemistry.chemical_compoundNon-alcoholic Fatty Liver DiseaseIFG Impaired Fasting GlucoseAPOB Apolipoprotein BNonalcoholic fatty liver diseasePIP Phosphatidyl-Inositol-PhosphateSteatohepatitisqRT-PCR quantitative Real Time Polymerase Chain ReactionMice Knockoutlcsh:R5-920ORO Oil Red O StainingPI PhosphatidylinositolFatty liverTM6SF2 Transmembrane 6 Superfamily Member 2PhospholipidTAG TriglyceridesNASH Nonalcoholic SteatohepatitisLipogenesisLPA Lyso-Phosphatidic AcidPhosphatidylinositolSignal TransductionPS Phosphatidyl-SerinePA Palmitic AcidALD alcoholic liver diseasePC Phosphatidylcholinei.v. IntravenousFATP1 Fatty Acid Transport Protein 1Models BiologicalInternal medicinemedicineAnimalsNonalcoholic fatty liver diseasePPARα Peroxisome Proliferator-Activated Receptor alphaObesityG3P Glyceraldehyde-3-PhosphateSREBP1c Sterol Regulatory Element-Binding Protein 1HDL High Density Lipoproteinsbusiness.industryPI3K Phosphatidylinositol 3 KinaseMembrane ProteinsNHEJ Non-Homologues End JoiningPNPLA3 Patatin-like Phospholipase Domain-containing-3MTTP Microsomal Triglyceride Transfer ProteinLPIAT1 Lysophosphatidylinositol Acyltransferase 1TMC4 Transmembrane Channel-Like 4Disease Models AnimalGene Expression RegulationHepatocytesFOXA2 Forkhead Box A2mTOR mammalian target of RapamycinSteatosisInsulin ResistancebusinessPG Phosphatidyl-GlycerolFABP1 Fatty Acid-Binding Protein 1 FAS Fatty Acid SynthaseT2DM Type 2 Diabetes MellitusEBioMedicine
researchProduct

Expression of the ALS-causing variant hSOD1G93A leads to an impaired integrity and altered regulation of claudin-5 expression in an in vitro blood–sp…

2015

Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disorder characterized by progressive paralysis due to the loss of primary and secondary motor neurons. Mutations in the Cu/Zn-superoxide dismutase (SOD1) gene are associated with familial ALS and to date numerous hypotheses for ALS pathology exist including impairment of the blood–spinal cord barrier. In transgenic mice carrying mutated SOD1 genes, a disrupted blood–spinal cord barrier as well as decreased levels of tight junction (TJ) proteins ZO-1, occludin, and claudin-5 were detected. Here, we examined TJ protein levels and barrier function of primary blood–spinal cord barrier endothelial cells of presymptomatic hSOD1G93…

SOD1FOXO1Mice TransgenicBiologyOccludinCell LineMiceGene expressionAnimalsClaudin-5ClaudinProtein kinase BBarrier functionCells CulturedTight Junction ProteinsTight junctionSuperoxide DismutaseAmyotrophic Lateral SclerosisEndothelial CellsCell biologyDisease Models AnimalNeurologyGene Expression RegulationSpinal CordImmunologyOriginal ArticleNeurology (clinical)Cardiology and Cardiovascular MedicineSignal Transduction
researchProduct

Role of SIRT1 and FOXO factors in eNOS transcriptional activation by resveratrol.

2013

Many of the cardiovascular protective effects of resveratrol are attributable to an enhanced production of nitric oxide (NO) by the endothelial NO synthase (eNOS). Resveratrol has been shown to enhance eNOS gene expression as well as eNOS enzymatic activity. The aim of the present study was to analyze the molecular mechanisms of eNOS transcriptional activation by resveratrol. Treatment of human EA.hy 926 endothelial cells with resveratrol led to a concentration-dependent upregulation of eNOS expression. In luciferase reporter gene assay, resveratrol enhanced the activity of human eNOS promoter fragments (3500, 1600, 633 and 263bp in length, respectively), indicating that the proximal promot…

Transcriptional ActivationCancer Researchendocrine system diseasesNitric Oxide Synthase Type IIIPhysiologyClinical BiochemistryFOXO1ResveratrolBiochemistryCell LineTransactivationchemistry.chemical_compoundSirtuin 1EnosStilbenesHumansRNA Small Interferingskin and connective tissue diseasesPromoter Regions GeneticTranscription factorGene knockdownAnalysis of VariancebiologySirtuin 1Chemistryorganic chemicalsfood and beveragesForkhead Transcription Factorsbiology.organism_classificationMolecular biologyUp-RegulationNitric oxide synthaseResveratrolGene Knockdown Techniquesbiology.proteinhormones hormone substitutes and hormone antagonistsNitric oxide : biology and chemistry
researchProduct

Effects of combined hormone replacement therapy or its effective agents on the IGF-1 pathway in skeletal muscle.

2010

Objectives To investigate the effects of combined hormone replacement therapy (HRT) and its effective agents on the IGF-1 signaling pathway. Design and methods To examine the effects of HRT on skeletal muscle in vivo, we utilized pre- and post-intervention samples from a randomized double blinded trial with 50–57-year-old women. The intervention included the year-long use of either HRT preparation (2 mg 17β-estradiol, E2; 1 mg norethisterone acetate, NETA, n = 10) or placebo (CO, n = 9). Microarray technology and quantitative PCR (qPCR) were used to study the expression of insulin-like growth factor I (IGF-1) and its splice variants as well as IGF-1 receptor, Akt1, mTOR, FOXO1, FOXO3, atrog…

estradioliTranscription GeneticEndocrinology Diabetes and MetabolismMuscle Fibers SkeletalEstrogen receptorpostmenopausal womenMuscle ProteinsFOXO1Receptor IGF Type 10302 clinical medicineEndocrinologyProtein IsoformsTestosteroneInsulin-Like Growth Factor IReceptorRandomized Controlled Trials as Topic0303 health sciencesEstradiolMyogenesisForkhead Box Protein O1TOR Serine-Threonine KinasesEstrogen Replacement TherapyForkhead Box Protein O3Forkhead Transcription FactorsMiddle Agedmedicine.anatomical_structureReceptors EstrogenReceptors AndrogenFemalemedicine.medical_specialtynorethisterone acetate030209 endocrinology & metabolismBiologypostmenopausaalinen nainen03 medical and health sciencesInternal medicinemedicineHumansnoretisteroniasetaattiluurankolihasskeletal muscleMuscle SkeletalProtein kinase BPI3K/AKT/mTOR pathway030304 developmental biologyhormonikorvaushoitoSKP Cullin F-Box Protein LigasesSkeletal muscleAndrogen receptorNorethindrone AcetateEndocrinologyHormone replacement therapyIGF-1 signalointiNorethindroneIGF-1 signalingProto-Oncogene Proteins c-aktGrowth hormoneIGF research : official journal of the Growth Hormone Research Society and the International IGF Research Society
researchProduct