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  • High levels of glucose induce metabolic memory in cardiomyocyte via epigenetic histone H3 lysine 9 methylation. 22707199

    Diabetic patients continue to develop inflammation and cardiovascular complication even after achieving glycemic control, suggesting a metabolic memory. Metabolic memory is a major challenge in the treatment of diabetic complication, and the mechanisms underlying metabolic memory are not clear. Recent studies suggest a link between chromatin histone methylation and metabolic memory. In this study, we tested whether histone 3 lysine-9 tri-methylation (H3K9me3), a key epigenetic chromatin marker, was involved in high glucose (HG)-induced inflammation and metabolic memory. Incubating cardiomyocyte cells in HG resulted in increased levels of inflammatory cytokine IL-6 mRNA when compared with myocytes incubated in normal culture media, whereas mannitol (osmotic control) has no effect. Chromatin immunoprecipitation (ChIP) assays showed that H3K9me3 levels were significantly decreased at the promoters of IL-6. Immunoblotting demonstrated that protein levels of the H3K9me3 methyltransferase, Suv39h1, were also reduced after HG treatment. HG-induced apoptosis, mitochondrial dysfunction and cytochrome-c release were reversible. However, the effects of HG on the expression of IL-6 and the levels of H3K9me3 were irreversible after the removal of HG from the culture. These results suggest that HG-induced sustained inflammatory phenotype and epigenetic histone modification, rather than HG-induced mitochondrial dysfunction and apoptosis, are main mechanisms responsible for metabolic memory. In conclusion, our data demonstrate that HG increases expression of inflammatory cytokine and decreases the levels of histone-3 methylation at the cytokine promoter, and suggest that modulating histone 3 methylation and inflammatory cytokine expression may be a useful strategy to prevent metabolic memory and cardiomyopathy in diabetic patients.
    Document Type:
    Reference
    Product Catalog Number:
    05-1242
    Product Catalog Name:
    Anti-trimethyl-Histone H3 (Lys9) Antibody, clone 6F12-H4

  • Purification of Candida guilliermondii and Pichia ohmeri killer toxin as an active agent against Penicillium expansum. 19680874

    An antifungal assay with cell-free culture supernatant of Pichia ohmeri 158 and Candida guilliermondii P3 was tested against Penicillium expansum strain #2 at 25 degrees C by measuring hyphal length and percentage conidia germination. C. guilliermondii was more effective against P. expansum conidia germination (58.15% inhibition), while P. ohmeri showed higher inhibition of mycelial growth (66.17%), indicating a probable mechanism associated with killer activity. This killer toxin (molecular mass 3 kDa) was partially purified by normal phase HPLC, using TSKgel Amide-80 analytical and preparative columns. Compared with crude extract, the killer toxin eluted from the post analytical column significantly inhibited P. expansum:% inhibition rose from 42.16 to 90.93% (C. guilliermondii) and 39.32 to 91.12% (P. ohmeri) (p 0.05). The one-step purification process was adequate in isolating killer toxin from culture supernatant and also increased anti-Penicillium activity.
    Document Type:
    Reference
    Product Catalog Number:
    6500

  • Involvement of brain-derived neurotrophic factor and sonic hedgehog in the spinal cord plasticity after neurotoxic partial removal of lumbar motoneurons. 22579680

    Adult mammals could spontaneously achieve a partial sensory-motor recovery after spinal cord injury, by mechanisms including synaptic plasticity. We previously showed that this recovery is associated to the expression of synapsin-I, and that sonic hedgehog and Notch-1 could be also involved in plasticity. The role of brain-derived neurotrophic factor and glutamate receptors in regulating synaptic efficacy has been explored in the last decade but, although these mechanisms are now well-defined in the brain, the molecular mechanisms underlying the so called spinal learning are still less clear. Here, we measured the expression levels of choline acetyltransferase, synapsin-I, sonic hedgehog, Notch-1, glutamate receptor subunits (GluR1, GluR2, GluR4, NMDAR1) and brain-derived neurotrophic factor, in a motoneuron-depleted mouse spinal lesion model obtained by intramuscular injection of cholera toxin-B saporin. The lesion caused the down-regulation of the majority of analysed proteins. Moreover, we found that in lesioned but not in control spinal tissue, synapsin-I expression is associated to that of both brain-derived neurotrophic factor and sonic hedgehog, whereas GluR2 expression is linked to that of Shh. These results suggest that brain-derived neurotrophic factor and sonic hedgehog could collaborate in modulating synaptic plasticity after the removal of motoneurons, by a mechanism involving both pre- and post-synaptic processes. Interestingly, the involvement of sonic hedgehog showed here is novel, and offers new routes to address spinal cord plasticity and repair.
    Document Type:
    Reference
    Product Catalog Number:
    07-218
    Product Catalog Name:
    Anti-Notch1 Antibody, extracellular domain

  • Both ischemic preconditioning and ghrelin administration protect hippocampus from ischemia/reperfusion and upregulate uncoupling protein-2. 19772611

    A major endogenous protective mechanism in many organs against ischemia/reperfusion (I/R) injury is ischemic preconditioning (IPC). By moderately uncoupling the mitochondrial respiratory chain and decreasing production of reactive oxygen species (ROS), IPC reduces apoptosis induced by I/R by reducing cytochrome c release from the mitochondria. One element believed to contribute to reduce ROS production is the uncoupling protein UCP2 (and UCP3 in the heart). Although its implication in IPC in the brain has been shown in vitro, no in vivo study of protein has shown its upregulation. Our first goal was to determine in rat hippocampus whether UCP2 protein upregulation was associated with IPC-induced protection and increased ROS production. The second goal was to determine whether the peptide ghrelin, which possesses anti-oxidant and protective properties, alters UCP2 mRNA levels in the same way as IPC during protection.After global forebrain ischemia (15 min) with 72 h reperfusion (I/R group), we found important neuronal lesion in the rat hippocampal CA1 region, which was reduced by a preceding 3-min preconditioning ischemia (IPC+I/R group), whereas the preconditioning stimulus alone (IPC group) had no effect. Compared to control, UCP2 protein labelling increased moderately in the I/R (+39%, NS) and IPC+I/R (+28%, NS) groups, and substantially in the IPC group (+339%, P less than 0.05). Treatment with superoxide dismutase (10000 U/kg ip) at the time of a preconditioning ischemia greatly attenuated (-73%, P less than 0.001) the increase in UCP2 staining at 72 h, implying a role of oxygen radicals in UCP2 induction.Hippocampal UCP2 mRNA showed a moderate increase in I/R (+33%, P less than 0.05) and IPC+I/R (+40%, P less than 0.05) groups versus control, and a large increase in the IPC group (+333%, P less than 0.001). In ghrelin experiments, the I/R+ghrelin group (3 daily administrations) showed considerable protection of CA1 neurons versus I/R animals, and increased hippocampal UCP2 mRNA (+151%, P less than 0.001).We confirm that IPC causes increased expression of UCP2 protein in vivo, at a moment appropriate for protection against I/R in the hippocampus. The two dissimilar protective strategies, IPC and ghrelin administration, were both associated with upregulated UCP2, suggesting that UCP2 may often represent a final common pathway in protection from I/R.
    Document Type:
    Reference
    Product Catalog Number:
    MAB377
    Product Catalog Name:
    Anti-NeuN Antibody, clone A60

  • Downregulation of miR-132 by promoter methylation contributes to pancreatic cancer development. 21665894

    MicroRNAs (miRNAs), which regulate gene expression by partial complementarity to the 3' untranslated region of their target genes, have been implicated in cancer initiation and progression. However, the molecular mechanism underlying the regulation of miRNA expression during pancreatic tumorigenesis has not been extensively reported. In this study, we first compared the miRNA expression in human pancreatic cancers and adjacent normal tissues by miRNA array and identified 12 differentially expressed miRNAs. miR-132, which is downregulated in tumors, was further studied in greater detail. Decreased expression of miR-132 was confirmed in 16 of 20 pancreatic carcinomas (P < 0.0001), compared with their respective benign tissues by TaqMan miRNA assays. miR-132 expression was remarkably influenced by promoter methylation in PANC1 and SW1990 cells. Promoter hypermethylation was observed in tumor samples but not in the normal counterparts, and the expression of miR-132 negatively correlated with its methylation status (P = 0.013). miR-132 was transcribed by RNA polymerase II, and Sp1 played a major role in miR-132 transcription. The expression of Sp1 correlated with that of miR-132 in tissues. Moreover, cancerous tissues showed significantly lower Sp1-binding affinity to the miR-132 promoter, relative to non-tumor samples. Proliferation and colony formation of pancreatic cancer cells were suppressed in cells transfected with miR-132 mimics and enhanced in cells transfected with miR-132 inhibitor by negatively regulating the Akt-signaling pathway. Our present findings illustrate the mechanism driving miR-132 downregulation and the important role of miR-132 in pancreatic cancer development.
    Document Type:
    Reference
    Product Catalog Number:
    17-371
    Product Catalog Name:
    EZ-ChIP™

  • Peroxynitrite decomposition catalyst ameliorates renal damage and protein nitration in cisplatin-induced nephrotoxicity in rats. 15458572

    Oxidative stress is involved in cisplatin-nephrotoxicity. However, it has not completely established if reactive nitrogen species and nitrosative stress are involved in this experimental model. The purpose of this work was to study the role of peroxynitrite, a reactive nitrogen specie, in cisplatin-nephrotoxicity using the compound 5,10,15,20-tetrakis (4-sulfonatophenyl) porphyrinato iron (III) (FeTPPS), a soluble complex able to metabolize peroxynitrite.In rats treated with cisplatin (a single intraperitoneal dose of 7.5 mg/kg body weight), renal nitrosative stress was made evident by the increase in 3-nitrotyrosine on day 3. In addition, cisplatin-induced nephrotoxicity was evident by the histological damage of proximal tubular cells and by the increase in (a) serum creatinine, (b) blood urea nitrogen, and (c) urinary excretion of N-acetyl-beta-D-glucosaminidase and total protein. Cisplatin-induced nitrosative stress and nephrotoxicity were attenuated by FeTPPS-treatment (15 mg/kg body weight, intraperitoneally, every 12 hours for 3 days).Nitrosative stress is involved in cisplatin-induced nephrotoxicity in rats. Our data suggest that peroxynitrite is involved, at least in part, in cisplatin-induced nephrotoxicity and protein nitration.
    Document Type:
    Reference
    Product Catalog Number:
    06-284
    Product Catalog Name:
    Anti-Nitrotyrosine Antibody

  • iNOS activity is necessary for the cytotoxic and immunogenic effects of doxorubicin in human colon cancer cells. 19925669

    Doxorubicin is one of the few chemotherapeutic drugs able to exert both cytotoxic and pro-immunogenic effects against cancer cells. Following the drug administration, the intracellular protein calreticulin is translocated with an unknown mechanism onto the plasma membrane, where it triggers the phagocytosis of tumour cells by dendritic cells. Moreover doxorubicin up-regulates the inducible nitric oxide (NO) synthase (iNOS) gene in cancer cells, leading to huge amounts of NO, which in turn acts as a mediator of the drug toxicity and as a chemosensitizer agent in colon cancer. Indeed by nitrating tyrosine on the multidrug resistance related protein 3, NO decreases the doxorubicin efflux from tumour cells and enhances the drug toxicity. It is not clear if NO, beside playing a role in chemosensitivity, may also play a role in doxorubicin pro-immunogenic effects. To clarify this issue, we compared the doxorubicin-sensitive human colon cancer HT29 cells with the drug-resistant HT29-dx cells and the HT29 cells silenced for iNOS (HT29 iNOS-).In both HT29-dx and HT29 iNOS- cells, doxorubicin did not induce NO synthesis, had a lower intracellular accumulation and a lower toxicity. Moreover the drug failed to promote the translocation of calreticulin and the phagocytosis of HT29-dx and HT29 iNOS-cells, which resulted both chemoresistant and immunoresistant. However, if NO levels were exogenously increased by sodium nitroprusside, the chemosensitivity to doxorubicin was restored in HT29 iNOS-cells. In parallel the NO donor per se was sufficient to induce the exposure of calreticulin and to increase the phagocytosis of HT29 iNOS- cells by DCs and their functional maturation, thus mimicking the pro-immunogenic effects exerted by doxorubicin in the parental drug-sensitive HT29 cells.Our data suggest that chemo- and immuno-resistance to anthracyclines are associated in colon cancer cells and rely on a common mechanism, that is the inability of doxorubicin to induce iNOS. Therefore NO donors might represent a promising strategy to restore both chemosensitivity and immunosensitivity to doxorubicin in resistant cells.
    Document Type:
    Reference
    Product Catalog Number:
    AB5411
    Product Catalog Name:
    Anti-Nitrotyrosine Antibody

  • Effect of different exercise modalities plus a hypocaloric diet on inflammation markers in overweight patients: a randomised trial. 23177481

    Inflammation markers (IM) have been associated with the development of chronic diseases. This study compares the effects on IM of three exercise programs combined with a hypocaloric diet.119 overweight participants (73 women, 46 men) aged 18-50 years were randomised into four treatment groups: strength training (S; n = 30), endurance training (E; n = 30), combined S + E (SE; n = 30), and a diet and physical activity recommendations group (D; n = 29). Energy intake, anthropometric variables (AV), training variables (VO2peak, strength index, dynamometric strength index [DSI]) and plasma IM were recorded at baseline and after 22 weeks of treatment.84 participants completed the study. At 22 weeks, all groups showed a significantly reduced energy intake (P < 0.001) and improved AV (P < 0.001). VO2peak significantly increased in all groups (P < 0.01). DSI increased in the exercise groups only (P < 0.05). Plasma leptin fell significantly (P < 0.001) in the S and E groups, but not significantly in the SE group (P = 0.029) (no significant differences between these groups). Tumour necrosis factor-α (TNF-α), and C-reactive protein (CRP) concentrations decreased in all groups when examined together, but not when examined separately. No significant differences were seen in interleukin-6 (IL-6).Combining strength or endurance training with a hypocaloric diet improved AV and reduced plasma leptin concentrations. No differences were seen between groups in terms of TNF-α, IL-6 or CRP reduction. This trial was registered at clinical trials.gov as NCT01116856. http://clinicaltrials.gov/.
    Document Type:
    Reference
    Product Catalog Number:
    HCCBP1MAG-58K
    Product Catalog Name:
    MILLIPLEX MAP Human Circulating Cancer Biomarker Magnetic Bead Panel - Cancer Multiplex Assay

  • Antitumor effect of all-trans retinoic acid-encapsulated nanoparticles of methoxy poly(ethylene glycol)-conjugated chitosan against CT-26 colon carcinoma in vitro. 18240304

    All-trans retinoic acid (ATRA)-incorporated nanoparticles of methoxy poly(ethylene glycol) (MPEG)-grafted chitosan were prepared through ion-complex formation between ATRA and chitosan. This nanoparticle has around 100 nm of diameter and favorable reconstitution properties. ATRA-incorporated nanoparticles has almost similar cytotoxicity against CT-26 tumor cells when compared to free ATRA. But nanoparticles was more effective to inhibit invasion of tumor cells than free ATRA at invasion test using matrigel. These results can be explained by apoptosis analysis using flow cytometer. When free ATRA or ATRA-incorporated nanoparticles were treated, tumor cells were slight progressed apoptosis. Furthermore, apoptosis was also progressed by treated with MPEG-grafted chitosan.
    Document Type:
    Reference
    Product Catalog Number:
    ECM550
    Product Catalog Name:
    QCM ECMatrix Cell Invasion Assay, 24-well (8 µm), colorimetric

  • Gradual loss of myelin and formation of an astrocytic scar during Wallerian degeneration in the human spinal cord. 14534158

    Axons undergo Wallerian degeneration distal to a point of injury. Experimental investigations have documented many of the cellular and molecular events that underlie this behaviour. Since relatively little is known about such events in human CNS pathologies and current experimental intervention strategies indicate the possibility of significant axon regeneration along the original degenerated fibre tract, we performed an immunohistochemical investigation of the dynamics of Wallerian degeneration in post mortem spinal cords of patients who died 2 days to 30 years after either cerebral infarction or traumatic spinal cord injury. Neurofilament (NF) staining demonstrated a spatio-temporal pattern of axonal loss within degenerating descending nerve fibre tracts that could be detected close to the lesion as early as 12 days after injury and progressed to an almost complete loss of NF immunoreactivity at survival times of 1 year and longer. Immunohistochemistry for glial fibrillary acidic protein revealed a late astrocytic reaction starting at 4 months after injury in the degenerating tracts, leading to the long-term deposition of a dense astrocytic scar. These events were accompanied by the gradual reduction of myelin basic protein in affected nerve fibre tracts, leading to almost complete loss by 3 years after injury. Since the extracellular matrix molecule chondroitin sulphate proteoglycan (CSPG) is known to be strongly inhibitory for axonal regeneration and to be a major component of gliotic scar tissues, we investigated the possible deposition of CSPG within the degenerating nerve fibre tracts. Apart from a local up-regulation close to the lesion site, our results show no enhanced CSPG expression within degenerated tracts at any survival time. This suggests that despite the apparent lack of CSPG in Wallerian degeneration, the slow reduction of CNS myelin and the long-term deposition of a dense astrocytic scar may present an environment that is non-supportive for axon regrowth.
    Document Type:
    Reference
    Product Catalog Number:
    AB980