AnatomyOrganismsDiseasesChemicals and DrugsAnalytical, Diagnostic and Therapeutic Techniques and EquipmentPhenomena and ProcessesDisciplines and OccupationsInformation Science
Endoplasmic Reticulum StressEndoplasmic ReticulumUnfolded Protein ResponseTranscription Factor CHOPActivating Transcription Factor 6TunicamycinCaspase 12Stress, PhysiologicalGlucoseMolecular ChaperonesActivating Transcription Factor 4ThapsigarginHeat-Shock ProteinsTaurochenodeoxycholic AcidEndoplasmic Reticulum, RoughApoptosisPhenylbutyrateseIF-2 KinaseProtein FoldingSarcoplasmic ReticulumEukaryotic Initiation Factor-2Golgi ApparatusBlood GlucoseMembrane ProteinsEndoplasmic Reticulum, SmoothSarcoplasmic Reticulum Calcium-Transporting ATPasesSignal TransductionEndoribonucleasesCell LineProtein TransportOxidative StressCells, CulturedCalreticulinCalciumCaspases, InitiatorInsulin-Secreting CellsCinnamatesGlucose Tolerance TestBrefeldin ABlotting, WesternCell Line, TumorCalnexinLiverMolecular Sequence DataAutophagyTranscription FactorsProtein Disulfide-IsomerasesGlucose IntoleranceMice, Inbred C57BLGene Expression RegulationIntracellular MembranesProteasome Endopeptidase ComplexGlycosylationMutationHSP70 Heat-Shock ProteinsCell DeathAmino Acid SequenceRNA, MessengerModels, BiologicalBiological TransportProtein Processing, Post-TranslationalHomeostasisCalcium-Transporting ATPasesMitochondriaThioureaCell SurvivalMice, KnockoutCell MembranePhosphorylationInsulinUp-RegulationProtein-Serine-Threonine KinasesTransfectionHeLa CellsDNA-Binding ProteinsSecretory PathwayReverse Transcriptase Polymerase Chain ReactionCCAAT-Enhancer-Binding ProteinsRNA, Small InterferingMicrosomesBasic-Leucine Zipper Transcription FactorsCaspasesCalcium SignalingMicroscopy, ElectronCarrier ProteinsTime FactorsReactive Oxygen SpeciesProtein BiosynthesisHep G2 CellsProtein BindingEnzyme InhibitorsCytosolMicroscopy, FluorescenceImmunoblottingHepatocytesMembrane GlycoproteinsSaccharomyces cerevisiaeDithiothreitolMice, TransgenicGlucose Transporter Type 1
OxidativeGRP78ApoptosisResponse to endoplasmicInflammationUptakeInducesPathwaysHomeostasisCellsProteinsPathwayDeprivationMetabolismInhibitionStarvationMitochondriaBlood glucose levelsInflammatoryAdipocytesPromotesIRE1MmolVitroATF6SecretionResident proteinTransporterCellularMarkersMetabolicVivoObeseCellSerumGeneHighRatsSignificantly higherLevels
Oxidative19
  • Oxidative stress is an important mechanism of neonatal hypoxic-ischemic brain damage. (frontiersin.org)
  • Furthermore, peroxisome proliferator-activated receptor γ-co-activator 1α (PGC-1α) is a key regulator of mitochondrial oxidative stress, which is regulated by Sirt1. (frontiersin.org)
  • Activation of Sirt1 with resveratrol improved cell's resistance to oxidative stress, whereas inhibition of Sirt1 with EX527 significantly reduced cell viability after cellular oxidative stress. (frontiersin.org)
  • In summary, these results confirmed that Sirt1 is a potent protective factor for neurons subjected to oxidative stress, and the protective effect of Sirt1 is attributed to its regulation of PGC-1α. (frontiersin.org)
  • Oxidative stress is one of the most important mechanisms of perinatal HI. (frontiersin.org)
  • Oxidative stress-mediated mitochondrial damage has been shown to be involved in apoptosis. (frontiersin.org)
  • RSV can improve mitochondrial function, reduce oxidative stress in podocytes, and inhibit apoptosis induction through the Sirt1/PGC-1a axis ( 12 ). (frontiersin.org)
  • Oxidative stress and mitochondrial dysfunction are important mechanisms of ventricular remodeling, predisposed to the development of diabetic cardiomyopathy (DCM) in type 2 diabetes mellitus. (mdpi.com)
  • In various mouse and rat models of obesity and type 1 and 2 diabetes mellitus, eCBs generated in various renal cells activate CB 1 receptors and contribute to the development of oxidative stress, inflammation, and renal fibrosis. (degruyter.com)
  • Oxidative protein folding by an endoplasmic reticulum-localized peroxiredoxin. (nih.gov)
  • In this review, we studied on the effects and molecular mechanisms of Rhizoma coptidis on NF-κB/MAPK/PI3K-Akt/AMPK/ERS and oxidative stress pathways. (springer.com)
  • Evidence presented in this review implicated that Rhizoma coptidis exerted beneficial effects on various diseases by regulation of NF-κB/MAPK/PI3K-Akt/AMPK/ERS and oxidative stress pathways, which support the clinical application of Rhizoma coptidis and offer references for future researches. (springer.com)
  • Oxidative stress pathways are caused by the imbalance of oxidation and antioxidation in body. (springer.com)
  • Oxidative stress pathways regulate redox balance by Nrf2 and other ways. (springer.com)
  • In this review, we sorted out the relationship of Rhizoma coptidis among components, diseases and NF-κB/MAPK/PI3K/Akt/AMPK/ERS/oxidative stress pathways, systematically studying on how Rhizoma coptidis exerts beneficial effects to various diseases, which supported the clinical application of Rhizoma coptidis and provided references for the future researches. (springer.com)
  • Various physiological and pathological conditions such as glucose starvation, inhibition of protein glycosylation and oxidative stress may cause an accumulation of unfolded proteins in the endoplasmic reticulum (ER), leading to the unfolded protein response (UPR) and autophagy. (spandidos-publications.com)
  • Several lines of evidence support a role for oxidative stress in the development of diabetes complications ( 13 , 14 ). (diabetesjournals.org)
  • Excess glucose is oxidized to FRUCTOSE depleting intracellular GLUTATHIONE, increasing susceptibility to oxidative stress. (thepmc.org)
  • Its pathophysiological mechanisms involve various biological events such as neuronal apoptosis, oxidative stress, endoplasmic reticulum stress and inflammatory cascade[ 2 - 5 ]. (ijpsonline.com)
GRP787
  • This agent induces cytotoxicity via ER stress pathway as shown by the increased expression of glucose-regulated protein-78 (GRP78), activating transcription factor 3 (ATF3), and C/EBP-homologous protein (CHOP). (cns.org)
  • Neuronal nitric oxide synthase (nNOS) and vitamin D receptor (VDR) expression were measured, as well as ER stress markers, including glucose-regulated protein78 (GRP78), protein kinase-like endoplasmic reticulum kinase (PERK) phosphorylation, eukaryotic initiation factor 2 alpha(eIF-2 alpha) phosphorylation, and CCAAT enhancer-binding protein homologous protein (CHOP). (cheric.org)
  • The molecular chaperone glucose-regulated protein 78 ( GRP78 ) or binding immunoglobulin protein (BiP), in addition to Ca 2+ binding and protein processing functions, possesses one more key role: master initiator of early UPR signaling. (molvis.org)
  • Western blot and immunohistochemistry were used to investigate the expression of ERp44 and Glucose-Regulated Protein 78(GRP78) in NPC. (biomedcentral.com)
  • We found the increased expression of ERp44 and GRP78 in NPC and ERp44 was highly expressed in ER-stressed tissues. (biomedcentral.com)
  • Intrathecal administration of Wnt signaling inhibitors (each at doses of 10 and 30 µM) in diabetic rats showed improvement in pain-associated behaviors (heat, cold & mechanical hyperalgesia) and nerve functions (motor, sensory nerve conduction velocities and nerve blood flow) by decreasing the expression of Wnt pathway proteins, inflammatory marker, matrix metalloproteinase 2 (MMP2), ER stress marker, glucose-regulated protein 78 (GRP78) and improving IENFD. (iasp-pain.org)
  • The glucose-regulated proteins (GRP78 and GRP94): functions, gene regulation, and applications. (prosci-inc.com)
Apoptosis1
  • The expressions of retinal GLP-1R, mitochondria-dependent apoptosis-associated genes, reactive gliosis markers, and endoplasmic reticulum stress-related pathway genes were studied by western blotting and immunohistochemistry in vivo and in vitro. (molvis.org)
Response to endoplasmic1
  • Mammalian transcription factor ATF6 is synthesized as a transmembrane protein and activated by proteolysis in response to endoplasmic stress. (prosci-inc.com)
Inflammation3
Uptake11
  • Therefore, cells with higher glucose uptake, for example tumor cells, have also a higher uptake of 2-DG. (wikipedia.org)
  • This is increasingly done in tandem with a CT function which is part of the same PET/CT machine, to allow better localization of small-volume tissue glucose-uptake differences. (wikipedia.org)
  • This study aimed to determine whether I3C or DIM could increase glucose uptake via enhanced insulin sensitivity in 3T3‐L1 adipocytes, as well as the mechanism involved. (researchgate.net)
  • DIM also enhanced glucose uptake by increasing expression of glucose transporter 4 in adipocytes. (researchgate.net)
  • Conclusions Our findings suggest that DIM may improve insulin sensitivity through the activation of the insulin signaling pathway, leading to enhanced glucose uptake. (researchgate.net)
  • Previous studies have found that DIM can improve type 2 diabetes by enhancing glucose uptake through the activation of insulin signaling in 3T3-L1 cells, and by lowering the plasma glucose levels in high-fat-diet-fed obese mice [13, 14]. (researchgate.net)
  • DIM, a major metabolite of indole-3-carbinol, which is naturally produced in broccoli and cabbage, enhances glucose uptake through the improvement of insulin sensitivity in 3T3-L1 cells [13] . (researchgate.net)
  • 3,3′-diindolylmethane (DIM)-a natural compound produced from indole-3-carbinol, found in cruciferous vegetables-enhances glucose uptake by increasing the activation of the insulin signaling pathway in 3T3-L1 adipocytes. (researchgate.net)
  • serine residues and impairing insulin PI3K/Akt signaling, leading to decreased glucose uptake by adipocytes. (bioinf.org)
  • Rb1 shows anti-obesity and antihyperlycemic effects by reducing food intake and body weight in rats [15] and enhancing insulin-mediated glucose uptake in 3T3-L1 adipocytes [16], demonstrating its antidiabetic effect. (bioinf.org)
  • Cardiolipin depletion in brown and beige fat abolishes adipose thermogenesis and glucose uptake, which renders animals insulin resistant. (ku.dk)
Induces3
  • Because of its structural similarity to mannose, 2DG has the potential to inhibit N-glycosylation in mammalian cells and other systems, and as such induces ER stress and the Unfolded Protein Response (UPR) pathway. (wikipedia.org)
  • CONCLUSIONS- Collectively, these data suggest that high glucose induces TLR2 and -4 expression via PKC-α and PKC-δ, respectively, by stimulating NADPH oxidase in human monocytes. (diabetesjournals.org)
  • Standard of care for glioblastoma (GB), consisting of cytotoxic chemotherapy, steroids, and high-dose radiation, induces changes in the tumor microenvironment through its effects on glucose availability, which is a determinant for tumor progression (TP). (surgicalneurologyint.com)
Pathways2
Homeostasis6
Cells17
  • Cells were cultured at 37°C with 5% CO 2 in 10% FBS of the medium, including DMEM (low glucose), 100 U/mL penicillin, and 100 mg/mL streptomycin. (hindawi.com)
  • Endoplasmic reticulum oxidoreductin-1-like β (ERO1lβ) regulates susceptibility to endoplasmic reticulum stress and is induced by insulin flux in β-cells. (nih.gov)
  • HCT 116 colon cancer cells were exposed to purvalanol, which activated ER stress via upregulation of PERK, IRE1α gene expression, eIF-2α phosphorylation and ATF-6 cleavage at early time-points in the HCT 116 colon cancer cells. (spandidos-publications.com)
  • Glucose-dependent insulinotropic polypeptide (GIP) is a 42-amino acid incretin hormone that binds to a seven-transmembrane G-protein-coupled receptor (GIP-R) that is expressed in numerous tissues including islet β-cells and α-cells ( 1 , 2 ). (diabetesjournals.org)
  • Thus, in the present study, we examined TLR2 and TLR4 mRNA and protein expression and mechanism of their induction in monocytic cells under high-glucose conditions. (diabetesjournals.org)
  • High glucose increased TLR expression, myeloid differentiation factor 88, interleukin-1 receptor-associated kinase-1, and nuclear factor-κB (NF-κB) p65-dependent activation in THP-1 cells. (diabetesjournals.org)
  • Small inhibitory RNA to p47Phox in THP-1 cells abrogated high-glucose-induced TLR2 and TLR4 expression. (diabetesjournals.org)
  • To assess the therapeutic potential of naringin and the mechanisms involved, we cultured rat glomerular mesangial cells and grouped them according to different glucose concentrations, different action times, different concentrations of MCC950, and different concentrations of naringin.The cell proliferation was measured by MTT assay. (biomedcentral.com)
  • The expressions of NLRP3, ASC, caspase-1, IL-1β, and IL-18 in rat glomerular mesangial cells were significantly higher in the high glucose (HG) group than in the control normal glucose (NG) group and exhibited time-dependence activity. (biomedcentral.com)
  • Naringin inhibited the proliferation of cells that were induced by high glucose. (biomedcentral.com)
  • Our data suggested that exosomal ERp44 derived from ER-stressed NPC cells took an inevitable role in NPC chemoresistance and might act as a treatment target. (biomedcentral.com)
  • Rb1 and CK reversed these changes by inhibiting ER stress-induced swelling and ameliorating insulin resistance, therefore improving the insulin IRS-1/PI3K/Akt-signaling pathway in adipose cells. (bioinf.org)
  • Summary order MK-8776 Rb1 and CK inhibited swelling and improved insulin signaling in adipose cells by suppressing ER stress-associated NLRP3 swelling activation. (bioinf.org)
  • Overeating stresses the membrane network within cells called the endoplasmic reticulum (ER). (hopeobesitycentre.com)
  • Similar results were found in primary rat Müller cells under high glucose culture in vitro. (molvis.org)
  • Currently, we are investigating roles of IGF-1 signaling and stress responses in dystrophic muscle cells. (rosalindfranklin.edu)
  • Nevertheless increased expression of Hsp70 is observed in such cells following stress. (biovisi.com)
Proteins6
  • Endoplasmic reticulum stress (ERS) might be stimulated by a dysfunctional activity of ER dealing with the misfolded or unfold proteins [ 1 ]. (hindawi.com)
  • Lacking proteosomal function on aggregates of unfolded proteins, ER stress may induce autophagic machinery. (spandidos-publications.com)
  • Endoplasmic reticulum (ER) is an essential organelle responsible for protein synthesis, folding, post-translational modification of proteins and protein trafficking in eukaryotes ( 8 ). (spandidos-publications.com)
  • Hsp70, one class of stress proteins, is comprised of multiple members, all of which bind ATP in vitro, but are localized within different intracellular compartments. (biovisi.com)
  • XBP-1 Monoclonal Antibody: X box binding protein 1 (XBP-1) is a key protein in the mammalian unfolded protein response (UPR) that protects the cell against the stress of malfolded proteins in the endoplasmic reticulum (ER). (prosci-inc.com)
  • Together with other UPR transcription factors such as ATF6, XBP-1 stimulates the production of ER stress proteins including the ER resident protein chaperones glucose regulated protein (GRP) 78 and GRP94. (prosci-inc.com)
Pathway1
  • Thiazolidinedione activation (72 h) of this pathway in normal mouse islets caused a threefold increase of GIP-R protein and a doubling of insulin secretion to 16.7 mmol/l glucose/10 nmol/l GIP. (diabetesjournals.org)
Deprivation3
  • Our study shows that the expression of Sirt1 was downregulated after oxygen-glucose deprivation. (frontiersin.org)
  • ER alerts a self-protective mechanism that is called ER stress during nutrient deprivation, pathogen infection, alterations in redox status, intraluminal Ca 2+ levels and folding defective protein conditions ( 9 ). (spandidos-publications.com)
  • Cellular stress conditions such as glucose deprivation, depletion of ER calcium sto. (jscimedcentral.com)
Metabolism3
  • Our study showed that treated with appropriate concentration of active vitamin D could decrease the number of pathological pyramidal neurons, improve hippocampal nerve metabolism, and reduce the over-expression of nNOS, along with the relieved activation of ER stress in hippocampus of diabetic rats. (cheric.org)
  • These results suggest that 1,25-dihydroxy vitamin D-3 treatment can ameliorate hyperglycemia-induced damage on hippocampal metabolism, possibly through alleviating the aberrant activation of ER stress. (cheric.org)
  • Similarly, ginsenoside CK also exerts beneficial effects on glucose and lipid rate of metabolism, as well as insulin level of sensitivity in diabetic rats [17]. (bioinf.org)
Inhibition2
  • In today's study, we induced ER stress-associated irritation by revealing adipose adipocytes or tissues to high blood sugar insult, and observed the consequences of ginsenoside Rb1 and its own order MK-8776 metabolite CK on insulin PI3K signaling, with focus on the Rabbit polyclonal to TIMP3 inhibition of NLRP3 inflammasome activation in the placing of ER tension. (bioinf.org)
  • In addition, they create a large production of reactive oxygen species, which leads to the production of cytokines, macrophage recruitment, and inhibition of glucose transport 4 (GLUT-4), along with a deficiency in insulin signaling and the hormones leptin and adiponectin. (medscape.com)
Starvation1
  • Several physiological stresses including nutrient starvation, hypoxia, reactive oxygen species (ROS) production, pathogenic infections, and chemotherapy can trigger phagophore formation. (hindawi.com)
Mitochondria2
Blood glucose levels2
Inflammatory2
  • Additional studies revealed that PKC-α, PKC-δ, and p47Phox knockdown significantly abrogated high-glucose-induced NF-κB activation and inflammatory cytokine secretion. (diabetesjournals.org)
  • High glucose has been shown to induce inflammatory cytokines, chemokines, p38 mitogen-activated protein kinase, reactive oxygen species (ROS), protein kinase C (PKC), and nuclear factor-κB (NF-κB) activity in both clinical and experimental systems ( 7 - 12 ). (diabetesjournals.org)
Adipocytes1
  • Crls1 deficiency in thermogenic adipocytes diminishes inducible mitochondrial uncoupling and elicits a nuclear transcriptional response through endoplasmic reticulum stress-mediated retrograde communication. (ku.dk)
Promotes1
IRE11
Mmol1
  • Cardiovascular disease rose progressively as fasting plasma glucose and post-load glucose levels rose above 75 mg/dL = 4.2 mmol/liter (Coutinho M, Gerstein HC, Wang Y, Usuf S. The relationship between glucose and incident cardiovascular events. (thepmc.org)
Vitro1
  • In vitro , high glucose induced EndMT by increase of ENO1 levels. (ijbs.com)
ATF61
  • XBP1 mRNA is induced by ATF6 and spliced by IRE1p in response to ER stress to produce a highly active transcription factor. (prosci-inc.com)
Secretion2
  • In this ancillary study to the Restoring Insulin SEcretion (RISE) Study, we investigated the prevalence of and association with β-cell dysfunction of T+ and autoantibodies to the 65 kDa glutamic acid decarboxylase antigen (GADA) in obese pre-diabetes adults with impaired glucose tolerance (IGT) and recently diagnosed treatment naïve (Ndx) T2D. (frontiersin.org)
  • The Core performs assays and data interpretation for in vivo metabolic function tests, including IV, IP and oral glucose tolerance tests and insulin tolerance tests for parameters of insulin sensitivity, insulin secretion and glucose disposal. (mmpc.org)
Resident protein1
Transporter2
Cellular2
  • Cellular dynamics of KORRIGAN 1 (KOR1) is closely linked with cellulose biosynthesis and plant osmotic stress tolerance. (tamu.edu)
  • Cellular stress on the endoplasmic reticulum (ER) can contribute to various seemingly unrelated conditions, such as diabetes. (unboundsupplements.com)
Markers1
Metabolic1
  • Excess FFA increase the OXYGEN DEMANDS of ischemic heart muscle and reduce the use of glucose as a metabolic fuel by the heart. (thepmc.org)
Vivo1
  • The Core also provides ancillary services and procedures, including blood sampling for in vivo testing for glucose tolerance tests and insulin tolerance tests. (mmpc.org)
Obese1
  • Objective Indole‐3‐carbinol (I3C), a naturally occurring compound found in cruciferous vegetables, and its metabolite 3,3′‐diindolylmethane (DIM) reduce body mass and serum glucose levels in high‐fat‐diet‐induced obese mice. (researchgate.net)
Cell4
  • 2-DG is up taken by the glucose transporters of the cell. (wikipedia.org)
  • Moreover, we determined that during purvalanol-mediated ER stress, autophagic machinery was also activated prior to apoptotic cell death finalization. (spandidos-publications.com)
  • Hsp70 is typically not expressed in the cell under normal growth conditions, but is expressed at high levels in the cell experiencing stress. (biovisi.com)
  • Consequently, detection of Hsp70 using an antibody specific for the inducible form is quite useful in ascertaining whether a stress response has occurred in the cell. (biovisi.com)
Serum2
  • Fetal bovine serum (FBS), Dulbecco's modified Eagle's minimum essential medium (DMEM) (low glucose), penicillin, and streptomycin were purchased from Gibco (Life Technologies, NY, USA). (hindawi.com)
  • At the end of 12 weeks of treatment, the brains of the rats were analyzed by proton magnetic resonance spectroscopy (H-1-MRS). Rats were then weighed, tested for blood glucose, serum Ca, P, and vitamin D-3, and sacrificed for histopathological analysis of the hippo campus. (cheric.org)
Gene1
  • Gene Bank blast for a homologous nucleotide sequence revealed the same PPRE within the rat glucose-dependent insulinotropic polypeptide receptor (GIP-R) promoter sequence. (diabetesjournals.org)
High6
  • Diabetes mellitus (DM) is a non-communicable disease throughout the world in which there is persistently high blood glucose level from the normal range. (scielo.br)
  • 0.05) decrease in high-glucose-induced NF-κB activity, suggesting an additive effect. (diabetesjournals.org)
  • We investigated the expression of the NLRP3-inflammasome under high-glucose conditions, assessed the effects of naringin on that process, and further elucidated the role of naringin in the pathogenesis of diabetic kidney disease(DKD). (biomedcentral.com)
  • Lu L, Li X, Zhong Z, Zhou W, Zhou D, Zhu M, Miao C. KMT5A downregulation participated in High Glucose-mediated EndMT via Upregulation of ENO1 Expression in Diabetic Nephropathy. (ijbs.com)
  • Moreover, high glucose downregulated KMT5A levels and increased regulatory factor X1 (RFX1) levels. (ijbs.com)
  • KMT5A upregulation or si-RFX1 decreased high glucose-induced ENO1 expression and EndMT. (ijbs.com)
Rats1
  • Endoplasmic reticulum stress (ER stress) is involved in hippocampal lesion and promote diabetic neuropathy, so we focus on the effects of 1, 25-dihydroxy vitamin D-3 on ER stress in hippocampus of diabetic rats. (cheric.org)
Significantly higher1
  • T(+) NdxT2D were observed to have significantly higher fasting glucose ( p = 0.004), and 2 h glucose ( p = 0.0032), but significantly lower steady state C-peptide (sscpep, p = 0.007) compared to T(−) NdxT2D. (frontiersin.org)
Levels2