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  • 1.
    Autelli, Riccardo
    et al.
    Department of Experimental Medicine and Oncology, University of Turin, Italy.
    Ullio, Chiara
    Department of Experimental Medicine and Oncology, University of Turin, Italy.
    Prigione, Elisa
    Department of Experimental Medicine and Oncology, University of Turin, Italy.
    Schiavone, Nicola
    Department of Experimental Medicine and Oncology, University of Florence, Italy.
    Brunk, Ulf
    Linköping University, Department of Medicine and Care, Pharmacology. Linköping University, Faculty of Health Sciences.
    Capaccioli, Sergio
    Department of Experimental Medicine and Oncology, University of Florence, Italy.
    Baccino, Francesco
    Department of Experimental Medicine and Oncology, University of Turin, Italy.
    Bonelli, Gabriella
    Department of Experimental Medicine and Oncology, University of Turin, Italy.
    Divergent pathways for TNF and C₂-ceramide toxicity in HTC hematoma cells2009In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1793, 1182-1190 p.Article in journal (Refereed)
    Abstract [en]

    We previously showed that, in the rat hepatoma cell line HTC, TNF brings about a non-caspase-dependent, apoptosis-like process requiring NADPH oxidase activity, an iron-mediated pro-oxidant status, and a functional acidic vacuolar compartment. This process may thus involve mechanisms such as autophagy or relocation of lysosomal enzymes, perhaps secondary to the formation of ceramide by acidic sphingomyelinase. Here we investigated whether ceramide formation contributes to the apoptogenic process. HTC cells were found to be sensitive to exogenous ceramide and significantly protected against TNF by desipramine, an inhibitor of lysosomal acid sphingomyelinase. However, Bcl-2 transfection and Bcl-x(L) upregulation by dexamethasone significantly diminished the apoptogenic effect of ceramide but not that of TNF, suggesting that ceramide is not directly involved in TNF toxicity. Moreover, Bcl-x(L) silencing precluded dexamethasone-induced protection against ceramide and, by itself, induced massive death, demonstrating the strict dependence of HTC cells on Bcl-x(L) for survival also under standard culture conditions.

  • 2.
    Damdimopoulos, Anastasios E.
    et al.
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Gustafsson, Jan-Åke
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden.
    Spyrou, Giannis
    Department of Biosciences at Novum, Karolinska Institute, Huddinge, Sweden / Foundation for Biomedical Research, Academy of Athens, Athens, Greece.
    Nuclear immobilization of DsRed1 tagged proteins: a novel tool for studying DNA-protein interactions?2007In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1773, no 6, 687-690 p.Article in journal (Refereed)
    Abstract [en]

    DsRed1 is a red fluorescent protein that can be used as a fusion partner with other proteins to determine their subcellular localization, similarly to the popular green fluorescent proteins (GFP). Here, we report that fusion of DsRed1 to estrogen receptor alpha (ER alpha) renders the transcription factor immobile within the nucleus. Furthermore, we show that the immobilization is dependent on DNA interaction and that the binding to the DNA can be direct as well as indirect for DsRed to immobilize with its fusion partners. This observation could provide a new tool to be used for the identification of target genes containing low affinity binding sites for several transcription factors including ER alpha. In addition, it could be employed for studies on protein-DNA interactions as well as protein-protein interactions during protein complex formation on chromatin in the event of transcription initiation and regulation.

  • 3.
    Friederich, Malou
    et al.
    Uppsala universitet, Integrativ Fysiologi.
    Fasching, Angelica
    Uppsala universitet, Integrativ Fysiologi.
    Hansell, Peter
    Uppsala universitet, Integrativ Fysiologi.
    Nordquist, Lina
    Uppsala universitet, Integrativ Fysiologi.
    Palm, Fredrik
    Uppsala universitet, Integrativ Fysiologi.
    Diabetes-induced up-regulation of uncoupling protein-2 results in increased mitochondrial uncoupling in kidney proximal tubular cells2008In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1777, no 7-8, 935-940 p.Article in journal (Refereed)
    Abstract [en]

    We have previously reported increased O(2) consumption unrelated to active transport by tubular cells and up-regulated mitochondrial uncoupling protein (UCP)-2 expressions in diabetic kidneys. It is presently unknown if the increased UCP-2 levels in the diabetic kidney results in mitochondrial uncoupling and increased O(2) consumption, which we therefore investigated in this study. The presence of UCP-2 in proximal tubular cells was confirmed by immunohistochemistry and found to be increased (western blot) in homogenized tissue and isolated mitochondria from kidney cortex of diabetic rats. Isolated proximal tubular cells had increased total and ouabain-insensitive O(2) consumption compared to controls. Isolated mitochondria from diabetic animals displayed increased glutamate-stimulated O(2) consumption (in the absence of ADP and during inhibition of the ATP-synthase by oligomycin) compared to controls. Guanosine diphosphate, an UCP inhibitor, and bovine serum albumin which removes fatty acids that are essential for UCP-2 uncoupling activity, independently prevented the increased glutamate-stimulated O(2) consumption in mitochondria from diabetic animals. In conclusion, diabetic rats have increased mitochondrial UCP-2 expression in renal proximal tubular cells, which results in mitochondrial uncoupling and increased O(2) consumption. This mechanism may be protective against diabetes-induced oxidative stress, but will increase O(2) usage. The subsequently reduced O(2) availability may contribute to diabetes-induced progressive kidney damage.

  • 4.
    Ghavami, Saeid
    et al.
    Department of Physiology, University of Manitoba, Canada.
    Cunnington, Ryan H
    Institute of Cardiovascular Sciences, University of Manitoba, Canada.
    Yeganeh, Behzad
    Department of Physiology, University of Manitoba, Canada.
    Davies, Jared J L
    Institute of Cardiovascular Sciences, University of Manitoba, Canada.
    Rattan, Sunil G
    Institute of Cardiovascular Sciences, University of Manitoba, Canada.
    Bathe, Krista
    Institute of Cardiovascular Sciences, University of Manitoba, Canada.
    Kavosh, Morvarid
    Institute of Cardiovascular Sciences, University of Manitoba, Canada.
    Los, Marek J
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Cell Biology.
    Freed, Darren H
    Department of Physiology, University of Manitoba, Canada.
    Klonisch, Thomas
    Department of Human Anatomy and Cell Science, University of Manitoba, Canada.
    Pierce, Grant N
    Department of Physiology, University of Manitoba, Canada.
    Halayko, Andrew J
    Department of Physiology, University of Manitoba, Canada.
    Dixon, Ian M C
    Department of Physiology, University of Manitoba, Canada.
    Autophagy regulates trans fatty acid-mediated apoptosis in primary cardiac myofibroblasts.2012In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1823, no 12, 2274-2286 p.Article in journal (Refereed)
    Abstract [en]

    Trans fats are not a homogeneous group of molecules and less is known about the cellular effects of individual members of the group. Vaccenic acid (VA) and elaidic acid (EA) are the predominant trans monoenes in ruminant fats and vegetable oil, respectively. Here, we investigated the mechanism of cell death induced by VA and EA on primary rat ventricular myofibroblasts (rVF). The MTT assay demonstrated that both VA and EA (200μM, 0-72h) reduced cell viability in rVF (P<0.001). The FACS assay confirmed that both VA and EA induced apoptosis in rVF, and this was concomitant with elevation in cleaved caspase-9, -3 and -7, but not caspase-8. VA and EA decreased the expression ratio of Bcl2:Bax, induced Bax translocation to mitochondria and decrease in mitochondrial membrane potential (Δψ). BAX and BAX/BAK silencing in mouse embryonic fibroblasts (MEF) inhibited VA and EA-induced cell death compared to the corresponding wild type cells. Transmission electron microscopy revealed that VA and EA also induced macroautophagosome formation in rVF, and immunoblot analysis confirmed the induction of several autophagy markers: LC3-β lipidation, Atg5-12 accumulation, and increased beclin-1. Finally, deletion of autophagy genes, ATG3 and ATG5 significantly inhibited VA and EA-induced cell death (P<0.001). Our findings show for the first time that trans fat acid (TFA) induces simultaneous apoptosis and autophagy in rVF. Furthermore, TFA-induced autophagy is required for this pro-apoptotic effect. Further studies to address the effect of TFA on the heart may reveal significant translational value for prevention of TFA-linked heart disease.

  • 5.
    Ghavami, Saeid
    et al.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Mutawe, Mark M.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Hauff, Kristin
    Department of Pharmacology, University of Manitoba, Winnipeg, MB, Canada.
    Stelmack, Gerald L.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Schaafsma, Dedmer
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Sharma, Pawan
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    McNeill, Karol D.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Hynes, Tyler S.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada.
    Kung, Sam K.
    Department of Immunology, University of Manitoba, Winnipeg, MB, Canada.
    Unruh, Helmut
    Department of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada.
    Klonisch, Thomas
    Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, MB, Canada.
    Hatch, Grant M.
    Department of Pharmacology, University of Manitoba, Winnipeg, MB, Canada.
    Los, Marek Jan
    Interfaculty Institute for Biochemistry, University of Tübingen, Germany.
    Halayko, Andrew J.
    Department of Physiology, University of Manitoba, Winnipeg, MB, Canada; National Training Program in Allergy and Asthma, University of Manitoba, Winnipeg, MB, Canada; Biology of Breathing Group, Manitoba Institute of Child Health, Winnipeg, MB, Canada; Department of Internal Medicine, University of Manitoba, Winnipeg, MB, Canada .
    Statin-triggered cell death in primary human lung mesenchyrnal cells involves p53-PUMA and release of Smac and Omi but not cytochrome c2010In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1803, no 4, 452-467 p.Article in journal (Refereed)
    Abstract [en]

    Statins inhibit 3-hydroxy-3-methyl-glutarylcoenzyme CoA (HMG-CoA) reductase, the proximal enzyme forcholesterol biosynthesis. They exhibit pleiotropic effects and are linked to health benefits for diseasesincluding cancer and lung disease. Understanding their mechanism of action could point to new therapies,thus we investigated the response of primary cultured human airway mesenchymal cells, which play aneffector role in asthma and chronic obstructive lung disease (COPD), to simvastatin exposure. Simvastatininduced apoptosis involving caspase-9, -3 and -7, but not caspase-8 in airway smooth muscle cells andfibroblasts. HMG-CoA inhibition did not alter cellular cholesterol content but did abrogate de novocholesterol synthesis. Pro-apoptotic effects were prevented by exogenous mevalonate, geranylgeranylpyrophosphate and farnesyl pyrophosphate, downstream products of HMG-CoA. Simvastatin increasedexpression of Bax, oligomerization of Bax and Bak, and expression of BH3-only p53-dependent genes, PUMAand NOXA. Inhibition of p53 and silencing of p53 unregulated modulator of apoptosis (PUMA) expressionpartly counteracted simvastatin-induced cell death, suggesting a role for p53-independent mechanisms.Simvastatin did not induce mitochondrial release of cytochrome c, but did promote release of inhibitor ofapoptosis (IAP) proteins, Smac and Omi. Simvastatin also inhibited mitochondrial fission with the loss ofmitochondrial Drp1, an essential component of mitochondrial fission machinery. Thus, simvastatin activatesnovel apoptosis pathways in lung mesenchymal cells involving p53, IAP inhibitor release, and disruption ofmitochondrial fission.

  • 6.
    Höst, Gunnar
    et al.
    Linköping University, Department of Physics, Chemistry and Biology, Molecular Biotechnology . Linköping University, The Institute of Technology.
    Jonsson, Bengt-Harald
    Linköping University, Department of Physics, Chemistry and Biology, Molecular Biotechnology . Linköping University, The Institute of Technology.
    Converting human carbonic anhydrase II into a benzoate ester hydrolase through rational redesign2008In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1784, no 5, 811-815 p.Article in journal (Refereed)
    Abstract [en]

    Enzymes capable of benzoate ester hydrolysis have several potential medical and industrial applications. A variant of human carbonic anhydrase II (HCAII) was constructed, by rational design, that is capable of hydrolysing para-nitrophenyl benzoate (pNPBenzo) with an efficiency comparable to some naturally occuring esterases. The design was based on a previously developed strategy,[1] in which docking of a transition state analogue (TSA) to the active site of HCAII was used to predict mutations that would allow the reaction. A triple mutant, V121A/V143A/T200A, was thus constructed and shown to hydrolyze pNPBenzo with kcat/KM = 625 (± 38) M-1s-1. It is highly active with other ester substrates as well, and hydrolyzes para-nitrophenyl acetate with kcat/KM = 101700 (± 4800) M-1s-1, which is the highest esterase efficiency so far for any CA variant. A parent mutant (V121A/V143A) has measurable KM values for para-nitrophenyl butyrate (pNPB) and valerate (pNPV),[1] but for V121A/V143A/T200A no KM could be determined, showing that the additional T200A mutation has caused a decreased substrate binding. However, kcat/KM is higher with both substrates for the triple mutant, indicating that binding energy has been diverted from substrate binding to transition state stabilization.

  • 7.
    Ljunggren, Stefan A
    et al.
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Levels, Johannes H M
    Academic Medical Centre, Amsterdam, the Netherlands.
    Hovingh, Kees
    Academic Medical Centre, Amsterdam, the Netherlands.
    Holleboom, Adriaan G
    Academic Medical Centre, Amsterdam, the Netherlands.
    Vergeer, Menno
    Academic Medical Centre, Amsterdam, the Netherlands.
    Argyri, Letta
    National Center for Scientific Research "Demokritos", Athens, Greece.
    Gkolfinopoulou, Christina
    National Center for Scientific Research "Demokritos", Athens, Greece.
    Chroni, Angeliki
    National Center for Scientific Research "Demokritos", Athens, Greece.
    Sierts, Jeroen A
    Academic Medical Centre, Amsterdam, the Netherlands.
    Kastelein, John J
    Academic Medical Centre, Amsterdam, the Netherlands.
    Kuivenhoven, Jan Albert
    University of Groningen, University Medical Center Groningen, Groningen, the Netherlands.
    Lindahl, Mats
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences.
    Karlsson, Helen
    Linköping University, Department of Clinical and Experimental Medicine, Division of Neuro and Inflammation Science. Linköping University, Faculty of Medicine and Health Sciences. Region Östergötland, Heart and Medicine Center, Occupational and Environmental Medicine Center.
    Lipoprotein profiles in human heterozygote carriers of a functional mutation P297S in scavenger receptor class B1.2015In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1851, no 12, 1587-1595 p.Article in journal (Refereed)
    Abstract [en]

    The scavenger receptor class B type 1 (SR-B1) is an important HDL receptor involved in cholesterol uptake and efflux, but its physiological role in human lipoprotein metabolism is not fully understood. Heterozygous carriers of the SR-B1P297S mutation are characterized by increased HDL cholesterol levels, impaired cholesterol efflux from macrophages and attenuated adrenal function. Here, the composition and function of lipoproteins were studied in SR-B1P297S heterozygotes.

    Lipoproteins from six SR-B1P297S carriers and six family controls were investigated. HDL and LDL/VLDL were isolated by ultracentrifugation and proteins were separated by two-dimensional gel electrophoresis and identified by mass spectrometry. HDL antioxidant properties, paraoxonase 1 activities, apoA-I methionine oxidations and HDL cholesterol efflux capacity were assessed.

    Multivariate modeling separated carriers from controls based on lipoprotein composition. Protein analyses showed a significant enrichment of apoE in LDL/VLDL and of apoL-1 in HDL from heterozygotes compared to controls. The relative distribution of plasma apoE was increased in LDL and in lipid-free form. There were no significant differences in paraoxonase 1 activities, HDL antioxidant properties or HDL cholesterol efflux capacity but heterozygotes showed a significant increase of oxidized methionines in apoA-I.

    The SR-B1P297S mutation affects both HDL and LDL/VLDL protein compositions. The increase of apoE in carriers suggests a compensatory mechanism for attenuated SR-B1 mediated cholesterol uptake by HDL. Increased methionine oxidation may affect HDL function by reducing apoA-I binding to its targets. The results illustrate the complexity of lipoprotein metabolism that has to be taken into account in future therapeutic strategies aiming at targeting SR-B1.

  • 8.
    Lundberg, Peter
    et al.
    Linköping University, Department of Medical and Health Sciences, Division of Radiological Sciences. Linköping University, Faculty of Health Sciences. Linköping University, Center for Medical Image Science and Visualization (CMIV). Region Östergötland, Center for Surgery, Orthopaedics and Cancer Treatment, Department of Radiation Physics. Department of Biological Sciences, University of Calgary, Calgary Canada.
    Vogel, Hans J.
    Department of Biological Sciences, University of Calgary, Calgary Canada.
    Drakenberg, Torbjörn
    Department of Physical Chemistry 2, University of Lund, Lund Sweden.
    Forsén, Sture
    Department of Physical Chemistry 2, University of Lund, Lund Sweden.
    Amiconi, Gino
    CNR Center of Molecular Biology and Department of Biochemical Sciences, Rome Italy.
    Forlani, Luciano
    Department of Experimental Medicine, University ‘La Sapienza’, Rome Italy.
    Chiancone, Emilia
    CNR Center of Molecular Biology and Department of Biochemical Sciences, Rome Italy.
    A35Cl--NMR study of the singular anion-binding properties of dromedary hemoglobin1989In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 999, no 1, 12-8 p.Article in journal (Refereed)
    Abstract [en]

    35Cl(-)-NMR measurements of chloride binding to carbonmonoxy- and deoxy-dromedary hemoglobin reveal the existence of two classes of chloride-binding sites, one of high and the other of low affinity. Although this situation resembles that described for human hemoglobin, it was found that the number of binding sites as well as the association equilibrium constant for chloride binding are significantly higher in the dromedary protein. This difference may be due to the greater number of basic residues exposed to solvent and to the higher flexibility of dromedary hemoglobin. The two oxygen-linked polyanion-binding sites characteristic of this hemoglobin show competition for some of the high-affinity chloride-binding sites in keeping with their location in the cleft enclosed by the beta chains and between the alpha chains termini. It is suggested that the observed anion-binding properties of dromedary hemoglobin may contribute to the control of the physiological osmotic shock after rehydration.

  • 9.
    Miranda-Vizuete, Antonio
    et al.
    Karolinska Institutet, Novum, Huddinge, Sweden.
    Damdimopoulos, Anastasios E.
    Karolinska Institutet, Novum, Huddinge, Sweden.
    Spyrou, Giannis
    Karolinska Institutet, Novum, Huddinge, Sweden.
    cDNA cloning, expression and chromosomal localization of the mouse mitochondrial thioredoxin reductase gene(1)1999In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1447, no 1, 113-118 p.Article in journal (Refereed)
    Abstract [en]

    Cytosolic thioredoxin (Trx) and thioredoxin reductase (TrxR) comprise a ubiquitous system that uses the reducing power of NADPH to act as a general disulfide reductase system as well as a potent antioxidant system. Human and rat mitochondria contain a complete thioredoxin system different from the one present in the cytosol. The mitochondrial system is involved in the oxidative stress protection through a mitochondrial thioredoxin-dependent peroxidase. We report here the cDNA cloning and chromosomal localization of the mouse mitochondrial thioredoxin reductase gene (TrxR2). The mouse TrxR2 cDNA encodes for a putative protein of 527 amino acid residues with a calculated molecular mass of 57 kDa, that displays high homology with the human and rat counterparts. The N-terminus of the protein displays typical features of a mitochondrial targeting sequence with absence of acidic residues and abundance of basic residues. Mouse TrxR2 also contains a stop codon in frame at the C-terminus of the protein, necessary for the incorporation of selenocysteine that is required for enzymatic activity. The typical stem-loop structure (SECIS element) that drives the incorporation of selenocysteine is identified in the 3'-UTR. Northern analysis of the mouse TrxR2 mRNA shows a similar pattern of expression with the human homologue, with higher expression in liver, heart and kidney. Finally, we have assigned the mouse TrxR2 gene to chromosome 16 mapping at 11.2 cM from the centromer and linked to the catechol-o-methyltransferase (comt) gene.

  • 10.
    Rydell, G E
    et al.
    Institut Curie, Centre de Recherche, Traffic, Signaling and Delivery Group, 26 rue d'Ulm, F-75248 Paris Cedex 05, France; CNRS UMR144, France.
    Svensson, Lennart
    Linköping University, Faculty of Health Sciences. Linköping University, Department of Clinical and Experimental Medicine, Division of Microbiology and Molecular Medicine.
    Larson, G
    Dept. of Clinical Chemistry and Transfusion Medicine, Sahlgrenska Academy at the University of Gothenburg, SE-413 45 Sweden.
    Johannes, L
    Institut Curie, Centre de Recherche, Traffic, Signaling and Delivery Group, 26 rue d'Ulm, F-75248 Paris Cedex 05, France; CNRS UMR144, France.
    Römer, W
    CNRS UMR144, France; Institute of Biology II, University of Freiburg, Schänzlestraβe 1, 79104 Freiburg, Germany; BIOSS Centre for Biological Signalling Studies, Synthetic Biology of Signalling Processes Group, University of Freiburg, Schänzlestraβe 18, 79104 Freiburg, Germany.
    Human GII.4 norovirus VLP induces membrane invaginations on giant unilamellar vesicles containing secretor gene dependent α1,2-fucosylated glycosphingolipids.2013In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1828, no 8, 1840-5 p.Article in journal (Refereed)
    Abstract [en]

    Norovirus is a non-enveloped virus causing acute gastroenteritis. For human norovirus, no simple cell culture system is available and consequently knowledge on cellular entry of the virus is limited. The virus binds to ABH histo-blood group glycans on glycoproteins and glycosphingolipids. Non-secretors, characterized by the lack of ABH histo-blood group glycans in the gastrointestinal tract, are resistant to most norovirus infections, suggesting that these glycans may be part of the viral receptor. Recent studies have shown that polyomavirus enters the cell via membrane invaginations induced by the multivalent binding of the virus to receptor glycosphingolipids. In this study, we have investigated whether norovirus has the ability to induce membrane invaginations on giant unilamellar vesicles (GUVs) containing purified glycosphingolipids. First, we characterized the glycosphingolipid binding pattern of VLPs from the Dijon strain (genogroup II.4), using thin-layer chromatography. The VLP recognized the ABH active glycosphingolipids H type 1, Lewis b, B type 1, A type 1 and A Lewis b, but not lactotetraosylceramide or Lewis a, typically found in non-secretors. The binding pattern to glycosphingolipids incorporated into GUVs was in full agreement with the thin-layer chromatography experiments. Upon binding to the vesicles, the VLPs formed highly mobile clusters on the surface of the GUVs. VLP containing tubular invaginations were seen on the GUVs containing glycosphingolipids recognized by the VLP. In conclusion, this study suggests that human norovirus has the ability to induce membrane curvature by binding to and clustering glycosphingolipids, which may reflect the first step in cellular entry of the virus.

  • 11.
    Söderström, Mats
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Wigren, Jane
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Surapureddi, Sailesh
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Glass, Christopher K
    University of California, San Diego, La Jolla, CA , USA.
    Hammarström, Sven
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Novel prostaglandin D2-derived activators of peroxisome proliferator-activated receptor-γ are formed in macrophage cell cultures2003In: Biochimica et Biophysica Acta, ISSN 0006-3002, E-ISSN 1878-2434, Vol. 1631, no 1, 35-41 p.Article in journal (Refereed)
    Abstract [en]

    Incubation of RAW 264.7 murine macrophages with 9,15-dihydroxy-11-oxo-, (5Z,9alpha,13E,15(S))-Prosta-5,13-dien-1-oic acid [prostaglandin D(2) (PGD(2))] induced formation of considerable peroxisome proliferator-activated receptor-gamma (PPARgamma) activity [Nature 391 (1998) 79]. Because PGD(2) itself is a poor PPARgamma ligand, we incubated RAW 264.7 macrophage cultures with prostaglandin D(2) for 24 h and studied the ability of the metabolites formed to activate PPARgamma. PGD(2) products were extracted and fractionated by reverse phase high-performance liquid chromatography. Chemical identification was achieved by UV spectroscopy, gas-liquid chromatography/mass spectrometry and chemical syntheses of reference compounds. PGD(2) was converted to eight products, six of which were identified. Ligand-induced interaction of PPARgamma with steroid receptor coactivator-1 was determined by glutathione-S-transferase pull-down assays and PPARgamma activation was investigated by transient transfection of RAW 264.7 macrophages. In addition to the previously known ligand 11-oxo-(5Z,9,12E,14Z)-Prosta-5,9,12,14-tetraen-1-oic acid (15-deoxy-delta(12,14)-PGJ(2)), a novel PPARgamma ligand and activator viz. 9-hydroxy-11-oxo-, (5Z,9alpha,12E,14Z)-Prosta-5,12,14-trien-1-oic acid (15-deoxy-delta(12,14)-PGD(2)) was identified. The biological significance of these results is currently under investigation.

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