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  • 1.
    Anderson, Emma S.
    et al.
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Bjartmar, Carl
    Department of Neurosciences, Lerner Research Institue, Cleveland Clinic Foundation, Cleveland, Ohio.
    Westermark, Gunilla
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Hildebrand, Claes
    Linköping University, Department of Biomedicine and Surgery, Cell biology. Linköping University, Faculty of Health Sciences.
    Molecular heterogeneity of oligodendrocytes in chicken white matter1999In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 27, no 1, p. 15-21Article in journal (Refereed)
    Abstract [en]

    The classical studies by Del Rio Hortega (Mem. Real. Soc. Espan. Hist. Nat. 14:40–122, 1928) suggest that the oligodendrocyte population includes four morphological subtypes. Recent data from the cat and the rat show that the anatomy of oligodendrocytes related to early myelinating prospective large fibers differs from that of oligodendrocytes related to late myelinating prospective small fibers. After application of a polyclonal antiserum to cryostat sections from the chicken CNS, we noted that glial cells in the spinal cord white matter had become labeled. Analysis of the occurrence and cellular localization of this immunoreactivity—the T4-O immunoreactivity—in the CNS of the adult chicken showed that T4-O immunoreactive cells are enriched in the ventral funiculus and superficially in the lateral funiculus of the spinal cord, where they are co-localized with large fibers. Double staining with T4-O antiserum and anti-GFAP or the lectin BSI-B4 revealed that T4-O immunoreactive cells are not astrocytes or microglia. Staining with anti-HSP108, a general marker for avian oligodendrocytes, showed that T4-O immunoreactivity defines an oligodendroglial subpopulation. A search for T4-O immunoreactivity in spinal cord white matter of some other vertebrates revealed that T4-O immunoreactive cells are not present in sections from fish, frog, turtle, rat, and rabbit spinal cord white matter. These results suggest the presence of a fiber size-related molecular heterogeneity among chicken white matter oligodendrocytes.

  • 2. Caddick, Jenny
    et al.
    Kingham, Paul J
    Gardiner, Natalie J
    Wiberg, Mikael
    Umeå University, Faculty of Medicine, Integrative Medical Biology, Anatomy. Umeå University, Faculty of Medicine, Surgical and Perioperative Sciences, Hand Surgery.
    Terenghi, Giorgio
    Phenotypic and functional characteristics of mesenchymal stem cells differentiated along a Schwann cell lineage.2006In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 54, no 8, p. 840-849Article in journal (Refereed)
    Abstract [en]

    We have investigated the phenotypic and bioassay characteristics of bone marrow mesenchymal stromal cells (MSCs) differentiated along a Schwann cell lineage using glial growth factor. Expression of the Schwann cell markers S100, P75, and GFAP was determined by immunocytochemical staining and Western blotting. The levels of the stem cell markers Stro-1 and alkaline phosphatase and the neural progenitor marker nestin were also examined throughout the differentiation process. The phenotypic properties of cells differentiated at different passages were also compared. In addition to a phenotypic characterization, the functional ability of differentiated MSCs has been investigated employing a co-culture bioassay with dissociated primary sensory neurons. Following differentiation, MSCs underwent morphological changes similar to those of cultured Schwann cells and stained positively for all three Schwann cell markers. Quantitative Western blot analysis showed that the levels of S100 and P75 protein were significantly elevated upon differentiation. Differentiated MSCs were also found to enhance neurite outgrowth in co-culture with sensory neurons to a level equivalent or superior to that produced by Schwann cells. These findings support the assertion that MSCs can be differentiated into cells that are Schwann cell-like in terms of both phenotype and function.

  • 3.
    Clausen, Fredrik
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Erlandsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Combination of Growth Factor Treatment and Scaffold Deposition Following Experimental Traumatic Brain Injury Show a Temporary Effect on Cellular Regeneration2013In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 61, p. S196-S196Article in journal (Other academic)
  • 4.
    Forsberg-Nilsson, Karin
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Erlandsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Biochemistry and Microbiology.
    Zhang, Xiao-Qun
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Ueda, Hideho
    Svensson, Kristian
    Nister, Monica
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Trapp, Bruce D.
    Peterson, Alan C.
    Westermark, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Oligodendrocyte precursor hypercellularity and abnormal retina development in mice overexpressing PDGF-B in myelinating tracts2003In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 41, no 3, p. 276-89Article in journal (Refereed)
    Abstract [en]

    Platelet-derived growth factor (PDGF) influences the generation of neurons and glia during embryogenesis and in early postnatal life. In an attempt to determine the consequences of an overexpression of PDGF-B during the first weeks of life, we targeted transgenic expression of a human PDGF-B cDNA to myelinating tracts using the promoter region of the myelin basic protein (MBP) gene. Transgenic mRNA and protein were expressed in the brain and the expression profile of the human PDGF-B during early postnatal development closely paralleled that of the endogenous mouse MBP gene. The gross morphological appearance of transgenic brains was normal but at the cellular level several phenotypic alterations could be identified. In white matter tracts such as the corpus callosum and cerebellar medulla, there was a marked hypercellularity. The number of oligodendrocyte precursors was increased and astrocytes were more abundant. In adult mice carrying the MBP-PDGF-B transgene, however, myelination appeared normal and the amount of oligodendrocytes was similar to that of control littermates. In addition to the phenotypic alterations in the brain, investigation of eye structure revealed a striking disorganization of retinal architecture. The retina was folded with cells collected in papillar or follicular-like structures. Retinal whole mount preparations after India ink perfusion revealed capillary disorganization with large-caliber vessels supporting only a few fine branches. Our observations strengthen the notion that PDGF is an important effector molecule in postnatal CNS development.

  • 5. Gunnarson, Eli
    et al.
    Zelenina, Marina
    Axehult, Gustav
    Song, Yutong
    Bondar, Alexander
    Krieger, Patrik
    Brismar, Hjalmar
    KTH, School of Engineering Sciences (SCI), Applied Physics, Cell Physics.
    Zelenin, Sergey
    Aperia, Anita
    Identification of a molecular target for glutamate regulation of astrocyte water permeability2008In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 56, no 6, p. 587-596Article in journal (Refereed)
    Abstract [en]

    Astrocytes play a key role for maintenance of brain water homeostasis, but little is known about mechanisms of short-term regulation of astrocyte water permeability. Here, we report that glutamate increases astrocyte water permeability and that the molecular target for this effect is the aquaporin-4 (AQP4) serine 111 residue, which is in a strategic position for control of the water channel gating. The glutamate effect involves activation of group I metabotropic glutamate receptors (mGluR), intracellular calcium release, and activation of calcium/calmodulin-dependent protein kinase II (CaMKII) and nitric oxide synthase (NOS). The physiological impact of our results is underlined by the finding that mGluR activation increases the rate of hypoosmotic tissue swelling in acute rat hippocampal slices. Cerebral ischemia is associated with an excessive release of glutamate, and in postischemic cerebral edema ablation of AQP4 attenuates the degree of damage. Thus, we have identified AQP4 as the molecular target for drugs that may attenuate the development of brain edema.

  • 6.
    Guzman, A.
    et al.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England..
    Lange, S.
    Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria..
    Silva, M. E.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England.;Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Univ Austral Chile, Inst Pharm, Fac Sci, Valdivia, Chile.;Ctr Interdisciplinary Studies Nervous Syst CISNe, Valdivia, Chile..
    Gonzalez, G. A.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England..
    Tempfer, H.
    Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Inst Tendon & Bone Regenerat, Salzburg, Austria.;Austrian Cluster Tissue Regenerat, Vienna, Austria..
    van Wijngaarden, P.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England.;Royal Victorian Eye & Ear Hosp, Melbourne, Vic, Australia.;Univ Melbourne, Ctr Eye Res Australia, Melbourne, Vic, Australia.;Univ Melbourne, Ophthalmol, Dept Surg, Melbourne, Vic, Australia..
    Zhao, C.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England..
    Rotheneichner, P.
    Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Inst Expt Neuroregenerat, Salzburg, Austria..
    Trost, A.
    Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Ophthalmol Optometry & Res Program Expt Ophthalmo, Salzburg, Austria..
    O'Sullivan, A.
    Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Inst Expt Neuroregenerat, Salzburg, Austria..
    Couillard-Despres, S.
    Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Inst Expt Neuroregenerat, Salzburg, Austria..
    Bieler, L.
    Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Paracelsus Med Univ, Inst Expt Neuroregenerat, Salzburg, Austria..
    Errea, O.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England..
    Mae, Maarja Andaloussi
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Andrae, Johanna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    He, Liqun
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Keller, A.
    Zurich Univ, Zurich Univ Hosp, Div Neurosurg, Zurich, Switzerland..
    Betsholtz, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology. Karolinska Inst, Div Vasc Biol, Dept Med Biochem & Biophys, Stockholm, Sweden..
    Aigner, L.
    Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria..
    Franklin, R. J. M.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England..
    Rivera, F. J.
    Univ Cambridge, Wellcome Trust & MRC Cambridge Stem Cell Inst, Cambridge, England.;Paracelsus Med Univ, Inst Mol Regenerat Med, Salzburg, Austria.;Spinal Cord Injury & Tissue Regenerat Ctr SCI TRe, Salzburg, Austria.;Univ Austral Chile, Inst Anat Histol & Pathol, Fac Med, Valdivia, Chile.;Ctr Interdisciplinary Studies Nervous Syst CISNe, Valdivia, Chile..
    Pericytes promote the generation of oligodendrocytes during remyelination2017In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 65, no S1, p. E541-E542Article in journal (Other academic)
  • 7. Hailer, NP
    et al.
    Järhult, Josef D
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Medical Sciences, Infectious Diseases.
    Nitsch, R
    Resting Microglial Cells in Vitro: Analysis of Morphology and Adhesion Molecule Expression in Organotypic Hippocampal Slice Cultures.1996In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 18, no 4, p. 319-31Article in journal (Refereed)
  • 8. Hede, Sanna-Maria
    et al.
    Hansson, Inga
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Afink, Gijs B
    Eriksson, Anna
    Nazarenko, Inga
    Andrae, Johanna
    Genove, Guillem
    Westermark, Bengt
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Genetics and Pathology.
    Nistér, Monica
    GFAP promoter driven transgenic expression of PDGFB in the mouse brain leads to glioblastoma in a Trp53 null background2009In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 57, no 11, p. 1143-1153Article in journal (Refereed)
    Abstract [en]

    Glioblastomas are the most common and malignant astrocytic brain tumors in human adults. The tumor suppressor gene TP53 is commonly mutated and/or lost in astrocytic brain tumors and the TP53 alterations are often found in combination with excessive growth factor signaling via PDGF/PDGFRalpha. Here, we have generated transgenic mice over-expressing human PDGFB in brain, under control of the human GFAP promoter. These mice showed no phenotype, but on a Trp53 null background a majority of them developed brain tumors. This occurred at 2-6 months of age and tumors displayed human glioblastoma-like features with integrated development of Pdgfralpha+ tumor cells and Pdgfrbeta+/Nestin+ vasculature. The transgene was expressed in subependymal astrocytic cells, in glia limitans, and in astrocytes throughout the brain substance, and subsequently, microscopic tumor lesions were initiated equally in all these areas. With tumor size, there was an increase in Nestin positivity and variability in lineage markers. These results indicate an unexpected plasticity of all astrocytic cells in the adult brain, not only of SVZ cells. The results also indicate a contribution of widely distributed Pdgfralpha+ precursor cells in the tumorigenic process.

  • 9.
    Keller, A.
    et al.
    Univ Zurich, Dept Neurosurg, Zurich, Switzerland..
    Zarb, Y.
    Univ Zurich, Dept Neurosurg, Zurich, Switzerland..
    Johannson, B.
    Gothenburg Univ, Dept Biochem & Cell Biol, Gothenburg, Sweden..
    Betsholtz, Christer
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Greter, M.
    Univ Zurich, Inst Expt Immunol, Zurich, Switzerland..
    Colonna, M.
    Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO USA..
    The role of microglia in microvascular calcification in the brain2017In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 65, no S1, p. E509-E509Article in journal (Other academic)
  • 10. Lange, S.
    et al.
    De La Fuente, A. Guzman
    Rotheneichner, P.
    van Wijngaarden, P.
    Gonzalez, G. A.
    Tempfer, H.
    Trost, A.
    Zhao, C.
    Couillard-Despres, S.
    Andrae, Johanna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Vascular Biology.
    Betsholtz, C.
    Franklin, R. J. M.
    Aigner, L.
    Rivera, F. J.
    CNS-pericytes promote oligodendrocyte fate decision and differentiation contributing to myelin development and repair2015In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 63, no S1, p. E289-E290, article id T10-14BArticle in journal (Other academic)
  • 11.
    Liu, Li
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neuroanatomy.
    Persson, Jonas
    Svensson, Mikael
    Aldskogius, Håkan
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neuroanatomy.
    Glial Cell Responses, Complement and Clusterin in the Central Nervous System Following Dorsal Root Transection1998In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 23, no 3, p. 221-238Article in journal (Refereed)
    Abstract [en]

    We have examined the glial cell response, the possible expression of compounds associated with the complement cascade, including the putative complement inhibitor clusterin, and their cellular association during Wallerian degeneration in the central nervous system. Examination of the proliferation pattern revealed an overall greater mitotic activity after rhizotomy, an exclusive involvement of microglia in this proliferation after peripheral nerve injury, but, in addition, a small fraction of proliferating astrocytes after rhizotomy. Immunostaining with the phagocytic cell marker ED1 gradually became very prominent after rhizotomy, possibly reflecting a response to the extensive nerve fiber disintegration. Lumbar dorsal rhizotomy did not induce endogenous immunoglobulin G (IgG) deposition or complement expression in the spinal cord dorsal horn, dorsal funiculus, or gracile nucleus. This is in marked contrast to the situation after peripheral nerve injury, which appears to activate the entire complement cascade in the vicinity of the central sensory processes. Clusterin, a multifunctional protein with complement inhibitory effects, was markedly upregulated in the dorsal funiculus in astrocytes. In addition, there was an intense induction of clusterin expression in the degenerating white matter in oligodendrocytes, possibly reflecting a degeneration process in these cells. The findings suggest that 1) complement expression by microglial cells is intimately associated with IgG deposition; 2) axotomized neuronal perikarya, but not degenerating central fibers, undergo changes which induce such deposition; and 3) clusterin is not related to complement expression following neuronal injury but participates in regulating the state of oligodendrocytes during Wallerian degeneration.

  • 12.
    Lööv, Camilla
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Erlandsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Molecular Mechanisms in Astrocytic Degradation2013In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 61, no S1, p. S81-S81Article in journal (Other academic)
  • 13.
    Lööv, Camilla
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Mitchell, Claire H.
    University of Pennsylvania.
    Simonsson, Martin
    Uppsala University, Science for Life Laboratory, SciLifeLab.
    Erlandsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Slow degradation in phagocytic astrocytes can be enhanced by lysosomal acidification2015In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 63, no 11, p. 1997-2009Article in journal (Refereed)
    Abstract [en]

    Inefficient lysosomal degradation is central in the development of various brain disorders, but the underlying mechanisms and the involvement of different cell types remains elusive. We have previously shown that astrocytes effectively engulf dead cells, but then store, rather than degrade the ingested material. In the present study we identify reasons for the slow digestion and ways to accelerate degradation in primary astrocytes. Our results show that actin-rings surround the phagosomes for long periods of time, which physically inhibit the phago-lysosome fusion. Furthermore, astrocytes express high levels of Rab27a, a protein known to reduce the acidity of lysosomes by Nox2 recruitment, in order to preserve antigens for presentation. We found that Nox2 colocalizes with the ingested material, indicating that it may influence antigen processing also in astrocytes, as they express MHC class II. By inducing long-time acidification of astrocytic lysosomes using acidic nanoparticles, we could increase the digestion of astrocyte-ingested, dead cells. The degradation was, however, normalized over time, indicating that inhibitory pathways are up-regulated in response to the enhanced acidification.

  • 14.
    Lööv, Camilla
    et al.
    Department of Neuroscience, Uppsala University.
    Mitchell, Claire H.
    Department of Anatomy and Cell Biology, University of Pennsylvania.
    Simonsson, Martin
    Luleå University of Technology, Department of Computer Science, Electrical and Space Engineering, Signals and Systems.
    Erlandsson, Anna
    Department of Neuroscience, Uppsala University.
    Slow degradation in phagocytic astrocytes can be enhanced by lysosomal acidification2015In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 63, no 11, p. 1997-2009Article in journal (Refereed)
    Abstract [en]

    Inefficient lysosomal degradation is central in the development of various brain disorders, but the underlying mechanisms and the involvement of different cell types remains elusive. We have previously shown that astrocytes effectively engulf dead cells, but then store, rather than degrade the ingested material. In the present study we identify reasons for the slow digestion and ways to accelerate degradation in primary astrocytes. Our results show that actin-rings surround the phagosomes for long periods of time, which physically inhibit the phago-lysosome fusion. Furthermore, astrocytes express high levels of Rab27a, a protein known to reduce the acidity of lysosomes by Nox2 recruitment, in order to preserve antigens for presentation. We found that Nox2 colocalizes with the ingested material, indicating that it may influence antigen processing also in astrocytes, as they express MHC class II. By inducing long-time acidification of astrocytic lysosomes using acidic nanoparticles, we could increase the digestion of astrocyte-ingested, dead cells. The degradation was, however, normalized over time, indicating that inhibitory pathways are up-regulated in response to the enhanced acidification.

  • 15.
    Nikitidou, Elisabeth
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    Söllvander, Sofia
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    Zyśk, Marlena
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    Söderberg, L.
    BioArctic Neurosci, Stockholm, Sweden..
    Sehlin, Dag
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    Lannfelt, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    Erlandsson, Anna
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Public Health and Caring Sciences, Geriatrics. Rudbeck Lab, Mol Geriatr, Uppsala, Sweden..
    The A beta protofibril selective antibody mAb158 prevents accumulation of A beta in astrocytes and rescues neurons from A beta induced apoptosis2017In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 65, no S1, p. E170-E170Article in journal (Other academic)
  • 16.
    Thored, Pär
    et al.
    Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, University Hospital, Lund, Sweden.
    Heldmann, Ursula
    Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, University Hospital, Lund, Sweden.
    Gomes-Leal, Walace
    Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, University Hospital, Lund, Sweden.
    Gisler, Ramiro
    Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, University Hospital, Lund, Sweden.
    Darsalia, Vladimer
    Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund, Sweden.
    Taneera, Jalal
    Department for Diabetes and Endocrinology, Clinical Research Centre, Malmö, Sweden.
    Nygren, Jens Martin
    Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund, Sweden.
    Jacobsen, Sten-Eirik W.
    Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund, Sweden.
    Ekdahl, Christine T.
    Laboratory of Neurogenesis and Cell Therapy, Section of Restorative Neurology, University Hospital, Lund, Sweden.
    Kokaia, Zaal
    Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund, Sweden.
    Lindvall, Olle
    Lund Strategic Research Center for Stem Cell Biology and Cell Therapy, Lund, Sweden.
    Long-term accumulation of microglia with proneurogenic phenotype concomitant with persistent neurogenesis in adult subventricular zone after stroke2009In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 57, no 8, p. 835-849Article in journal (Refereed)
    Abstract [en]

    Neural stem cells (NSCs) in the adult rat subventricular zone (SVZ) generate new striatal neurons during several months after ischemic stroke. Whether the microglial response associated with ischemic injury extends into SVZ and influences neuroblast production is unknown. Here, we demonstrate increased numbers of activated microglia in ipsilateral SVZ concomitant with neuroblast migration into the striatum at 2, 6, and 16 weeks, with maximum at 6 weeks, following 2 h middle cerebral artery occlusion in rats. In the peri-infarct striatum, numbers of activated microglia peaked already at 2 weeks and declined thereafter. Microglia in SVZ were resident or originated from bone marrow, with maximum proliferation during the first 2 weeks postinsult. In SVZ, microglia exhibited ramified or intermediate morphology, signifying a downregulated inflammatory profile, whereas amoeboid or round phagocytic microglia were frequent in the peri-infarct striatum. Numbers of microglia expressing markers of antigen-presenting cells (MHC-II, CD86) increased in SVZ but very few lymphocytes were detected. Using quantitative PCR, strong short- and long-term increase (at 1 and 6 weeks postinfarct) of insulin-like growth factor-1 (IGF-1) gene expression was detected in SVZ tissue. Elevated numbers of IGF-1-expressing microglia were found in SVZ at 2, 6, and 16 weeks after stroke. At 16 weeks, 5% of microglia but no other cells in SVZ expressed the IGF-1 protein, which mitigates apoptosis and promotes proliferation and differentiation of NSCs. The long-term accumulation of microglia with proneurogenic phenotype in the SVZ implies a supportive role of these cells for the continuous neurogenesis after stroke.

  • 17.
    Wicher, Grzegorz
    et al.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Cancer and Vascular Biology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Wallenquist, Ulrika
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Enoksson, M.
    Fuchs, B.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Husic, E.
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Hillered, Lars
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Neuroscience, Neurosurgery.
    Nilsson, G.
    Forsberg Nilsson, Karin
    Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Medicine, Department of Immunology, Genetics and Pathology, Cancer and Vascular Biology. Uppsala University, Science for Life Laboratory, SciLifeLab.
    Interleukin-33 in brain development and traumatic brain injury2013In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 61, no S1, p. S185-S185Article in journal (Other academic)
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    Titova, N.
    Mukhina, I.
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    Umeå University, Faculty of Medicine, Department of Integrative Medical Biology (IMB).
    Preoptic glycine receptors: possible mediators of neuron-glial interaction affecting social behavior in male rats2017In: Glia, ISSN 0894-1491, E-ISSN 1098-1136, Vol. 65, p. E298-E299Article in journal (Refereed)
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