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oligodendrocyte parenchymal cells

Ilias Kazanis, Kimberley A Evans, Evangelia Andreopoulou, Christina Dimitriou, Christos Koutsakis, Ragnhildur Thora Karadottir, Robin J M Franklin
Two populations of oligodendrogenic progenitors co-exist within the corpus callosum (CC) of the adult mouse. Local, parenchymal oligodendrocyte progenitor cells (pOPCs) and progenitors generated in the subependymal zone (SEZ) cytogenic niche. pOPCs are committed perinatally and retain their numbers through self-renewing divisions, while SEZ-derived cells are relatively "young," being constantly born from neural stem cells. We compared the behavior of these populations, labeling SEZ-derived cells using hGFAP:Cre(Ert2) mice, within the homeostatic and regenerating CC of the young-adult and aging brain...
March 14, 2017: Stem Cell Reports
For Yue Tso, Ashley Sawyer, Eun Hee Kwon, Victor Mudenda, Dianne Langford, You Zhou, John West, Charles Wood
BACKGROUND: Kaposi's sarcoma-associated herpesvirus (KSHV) is the causative agent of Kaposi's sarcoma (KS), one of the leading cancers in HIV patients in Zambia. KSHV was detected in the human central nervous system (CNS) by PCR, but tissue location and cell tropism for KSHV infection has not been established. Given the neurotropism exhibited by other herpesviruses and the frequent coinfection of HIV positive individuals with KSHV, we sought to determine whether the CNS can be infected by KSHV in HIV positive Zambian individuals...
December 8, 2016: Journal of Infectious Diseases
Jessica X Yuan, Fahad F Bafakih, James W Mandell, Bethany J Horton, Jennifer M Munson
Glioblastomas, the most common primary malignant brain tumors, have a distinct tissue microenvironment. Although non-neoplastic cells contribute to glioblastoma progression, very few quantitative studies have shown the effect of tumor microenvironmental influences on patient survival. We examined relationships of the cellular microenvironment, including astrocytes, microglia, oligodendrocytes, and blood vessels, to survival in glioblastoma patients. Using histological staining and quantitative image analyses, we examined the tumor-associated parenchyma of 33 patients and developed statistical models to predict patient outcomes based on the cellular picture of the tumor parenchyma...
December 1, 2016: Journal of Neuropathology and Experimental Neurology
Nina Wagenknecht, Birte Becker, Miriam Scheld, Cordian Beyer, Tim Clarner, Tanja Hochstrasser, Markus Kipp
There is a broad consensus that multiple sclerosis (MS) represents more than an inflammatory disease: it harbors several characteristic aspects of a classical neurodegenerative disorder, i.e., damage to axons, synapses, and nerve cell bodies. While several accepted paraclinical methods exist to monitor the inflammatory-driven aspects of the disease, techniques to monitor progression of early and late neurodegeneration are still in their infancy and have not been convincingly validated. It was speculated that the thalamus with its multiple reciprocal connections is sensitive to inflammatory processes occurring in different brain regions, thus acting as a "barometer" for diffuse brain parenchymal damage in MS...
September 2016: Journal of Molecular Neuroscience: MN
Zhenggang Zhang, Michael Chopp
Stroke activates neural stem cells in the ventricular-subventricular zone (V/SVZ) of the lateral ventricle, which increases neuroblasts and oligodendrocyte progenitor cells (OPCs). Within the ischemic brain, neural stem cells, neuroblasts and OPCs appear to actively communicate with cerebral endothelial cells and other brain parenchymal cells to mediate ischemic brain repair; however, stroke-induced neurogenesis unlikely plays any significant roles in neuronal replacement. In this mini-review, we will discuss recent findings how intercellular communications between stroke-induced neurogenesis and oligodendrogenesis and brain parenchymal cells could potentially facilitate brain repair processes...
September 2016: Journal of Stroke
Davide Lecca, Marta Fumagalli, Stefania Ceruti, Maria P Abbracchio
In the central nervous system (CNS), during both brain and spinal cord development, purinergic and pyrimidinergic signalling molecules (ATP, UTP and adenosine) act synergistically with peptidic growth factors in regulating the synchronized proliferation and final specification of multipotent neural stem cells (NSCs) to neurons, astrocytes or oligodendrocytes, the myelin-forming cells. Some NSCs still persist throughout adulthood in both specific 'neurogenic' areas and in brain and spinal cord parenchyma, retaining the potentiality to generate all the three main types of adult CNS cells...
August 5, 2016: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences
Tamio Ito, Kenichi Sato, Yoshimaru Ozaki, Taku Asanome, Hirohiko Nakamura, Shinya Tanaka, Taichi Kimura, Hiromi Kanno
INTRODUCTION: In benign pineal parenchymal tumors (PPTs), namely, pineocytoma(PC)and PPT of intermediate differentiation (PPTID), cytologic pleomorphism has occasionally been found;however, it is controversial as to whether the presence of pleomorphic cells leads to upgrading of tumors. We experienced a rare case of pleomorphic PPT in an elderly woman and compared it with a retrospective series of 12 PPTs (PC:3, PPTID:6, pineoblastoma[PB]:3)to evaluate the correlation between pleomorphism and the malignancy grade...
June 2016: No Shinkei Geka. Neurological Surgery
Jayshree Samanta, Ethan M Grund, Hernandez M Silva, Juan J Lafaille, Gord Fishell, James L Salzer
Enhancing repair of myelin is an important but still elusive therapeutic goal in many neurological disorders. In multiple sclerosis, an inflammatory demyelinating disease, endogenous remyelination does occur but is frequently insufficient to restore function. Both parenchymal oligodendrocyte progenitor cells and endogenous adult neural stem cells resident within the subventricular zone are known sources of remyelinating cells. Here we characterize the contribution to remyelination of a subset of adult neural stem cells, identified by their expression of Gli1, a transcriptional effector of the sonic hedgehog pathway...
October 15, 2015: Nature
Takashi Kanda
The pathological findings of natalizumab-associated progressive multifocal leukoencephalopathy (PML) are reviewed. In addition to the classical pathology of PML including the presence of enlarged abnormal astrocytes, intranuclear inclusions mainly found within large swollen oligodendrocytes and abundant myelin-laden macrophages/microglia, massive perivascular and parenchymal mononuclear cell infiltration was observed. The latter pathologic picture is that of immune reconstitution inflammatory syndrome (IRIS), and most of these infiltrating cells are CD8-positive T cells...
July 2015: Brain and Nerve, Shinkei Kenkyū No Shinpo
Béatrice Brousse, Karine Magalon, Pascale Durbec, Myriam Cayre
Myelin regeneration can occur in the brain following demyelination. Parenchymal oligodendrocyte progenitors (pOPC) are known to play a crucial role in this process. Neural stem cells (NSC) residing in the ventricular-subventricular zone (V-SVZ) also have the ability to generate oligodendrocytes but their contribution to endogenous myelin repair was so far considered to be negligible. Here, we addressed the relative contribution of pOPC and V-SVZ-derived neural progenitors (SVZdNP) to remyelination in cuprizone mouse models of acute or chronic corpus callosum (CC) demyelination...
2015: Biology Open
Steven A Goldman, Maiken Nedergaard, Martha S Windrem
As new methods for producing and isolating human glial progenitor cells (hGPCs) have been developed, the disorders of myelin have become especially compelling targets for cell-based therapy. Yet as animal modeling of glial progenitor cell-based therapies has progressed, it has become clear that transplanted hGPCs not only engraft and expand within murine hosts, but dynamically outcompete the resident progenitors so as to ultimately dominate the host brain. The engrafted human progenitor cells proceed to generate parenchymal astrocytes, and when faced with a hypomyelinated environment, oligodendrocytes as well...
August 2015: Glia
Iliana Michailidou, Helga E de Vries, Elly M Hol, Miriam E van Strien
Multiple sclerosis (MS) is a chronic inflammatory disorder of the central nervous system, leading to severe neurological deficits. Current MS treatment regimens, consist of immunomodulatory agents aiming to reduce the rate of relapses. However, these agents are usually insufficient to treat chronic neurological disability. A promising perspective for future therapy of MS is the regeneration of lesions with replacement of the damaged oligodendrocytes or neurons. Therapies targeting to the enhancement of endogenous remyelination, aim to promote the activation of either the parenchymal oligodendrocyte progenitor cells or the subventricular zone-derived neural stem cells (NSCs)...
2014: Frontiers in Neuroscience
Alexia Kagiava, Irene Sargiannidou, Stavros Bashiardes, Jan Richter, Natasa Schiza, Christina Christodoulou, Angela Gritti, Kleopas A Kleopa
BACKGROUND: Most leukodystrophies result from mutations in genes expressed in oligodendrocytes that may cause autonomous loss of function of cell structural proteins. Therefore, effective gene delivery to oligodendrocytes is necessary to develop future treatments. MATERIALS: To achieve this, we cloned a lentiviral vector in which the enhanced green fluorescent protein (EGFP) expression was driven by the oligodendrocyte specific 2,3-cyclic nucleotide 3-phosphodiesterase promoter...
November 2014: Journal of Gene Medicine
Yao Lulu Xing, Philipp T Röth, Jo Anne S Stratton, Bernard H A Chuang, Jill Danne, Sarah L Ellis, Sze Woei Ng, Trevor J Kilpatrick, Tobias D Merson
Parenchymal oligodendrocyte progenitor cells (pOPCs) are considered the principal cell type responsible for oligodendrogenesis and remyelinaton in demyelinating diseases. Recent studies have demonstrated that neural precursor cells (NPCs) from the adult subventricular zone (SVZ) can also generate new oligodendrocytes after demyelination. However, the relative contribution of NPCs versus pOPCs to remyelination is unknown. We used in vivo genetic fate mapping to assess the behavior of each progenitor type within the corpus callosi (CCs) of mice subjected to cuprizone-induced demyelination...
October 15, 2014: Journal of Neuroscience: the Official Journal of the Society for Neuroscience
Matthew C Tate, Robert A Lindquist, Thuhien Nguyen, Nader Sanai, A James Barkovich, Eric J Huang, David H Rowitch, Arturo Alvarez-Buylla
Despite its critical importance to global brain function, the postnatal development of the human pons remains poorly understood. In the present study, we first performed magnetic resonance imaging (MRI)-based morphometric analyses of the postnatal human pons (0-18 years; n = 6-14/timepoint). Pons volume increased 6-fold from birth to 5 years, followed by continued slower growth throughout childhood. The observed growth was primarily due to expansion of the basis pontis. T2-based MRI analysis suggests that this growth is linked to increased myelination, and histological analysis of myelin basic protein in human postmortem specimens confirmed a dramatic increase in myelination during infancy...
February 15, 2015: Journal of Comparative Neurology
Bilal El Waly, Magali Macchi, Myriam Cayre, Pascale Durbec
Oligodendrocytes (OLGs) are generated late in development and myelination is thus a tardive event in the brain developmental process. It is however maintained whole life long at lower rate, and myelin sheath is crucial for proper signal transmission and neuronal survival. Unfortunately, OLGs present a high susceptibility to oxidative stress, thus demyelination often takes place secondary to diverse brain lesions or pathologies. OLGs can also be the target of immune attacks, leading to primary demyelination lesions...
2014: Frontiers in Neuroscience
Sarah B Simmons, Denny Liggitt, Joan M Goverman
Multiple sclerosis (MS) is an autoimmune disease in which inflammatory lesions lead to tissue injury in the brain and/or spinal cord. The specific sites of tissue injury are strong determinants of clinical outcome in MS, but the pathways that determine whether damage occurs in the brain or spinal cord are not understood. Previous studies in mouse models of MS demonstrated that IFN-γ and IL-17 regulate lesion localization within the brain; however, the mechanisms by which these cytokines mediate their effects have not been identified...
July 15, 2014: Journal of Immunology: Official Journal of the American Association of Immunologists
Enrica Boda, Annalisa Buffo
NG2-expressing parenchymal precursors (NG2+p) serve as primary source of myelinating oligodendrocytes in both the developing and adult Central Nervous System (CNS). However, their abundance, limited differentiation potential at adult stages along with stereotypic reaction to injury independent of the extent of myelin loss suggest that NG2+p exert functions additional to myelin production. In support of this view, NG2+p express a complex battery of molecules known to exert neuromodulatory and neuroprotective functions...
2014: Frontiers in Neuroscience
Yoshihiko Hidaka, Yuji Inaba, Kazuyuki Matsuda, Makoto Itoh, Tomoki Kaneyama, Yozo Nakazawa, Chang-Sung Koh, Motoki Ichikawa
Multiple sclerosis (MS) is a chronic demyelinating disease often displaying a relapsing-remitting course of neurological manifestations that is mimicked by experimental autoimmune encephalomyelitis (EAE) in animal models of MS. In particular, NOD mice immunized with myelin oligodendrocyte glycoprotein peptide 35-55 develop chronic relapsing-remitting EAE (CREAE). To elucidate the mechanisms that cause MS relapse, we investigated the histopathology and cytokine production of spleen cells and mRNA expression levels in the central nervous system (CNS) of CREAE mice...
May 15, 2014: Journal of the Neurological Sciences
Debayon Paul, Shujun Ge, Yen Lemire, Evan R Jellison, David R Serwanski, Nancy H Ruddle, Joel S Pachter
BACKGROUND: Expression of chemokine CCL2 in the normal central nervous system (CNS) is nearly undetectable, but is significantly upregulated and drives neuroinflammation during experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis which is considered a contributing factor in the human disease. As astrocytes and brain microvascular endothelial cells (BMEC) forming the blood-brain barrier (BBB) are sources of CCL2 in EAE and other neuroinflammatory conditions, it is unclear if one or both CCL2 pools are critical to disease and by what mechanism(s)...
2014: Journal of Neuroinflammation
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