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  1. Article: Pharmacological Properties and Biological Functions of the GPR17 Receptor, a Potential Target for Neuro-Regenerative Medicine.

    Fumagalli, Marta / Lecca, Davide / Coppolino, Giusy T / Parravicini, Chiara / Abbracchio, Maria P

    Advances in experimental medicine and biology

    2017  

    Abstract: In 2006, cells heterologously expressing the "orphan" receptor GPR17 were shown to acquire responses to both uracil nucleotides and cysteinyl-leukotrienes, two families of signaling molecules accumulating in brain or heart as a result of hypoxic/ ... ...

    Abstract In 2006, cells heterologously expressing the "orphan" receptor GPR17 were shown to acquire responses to both uracil nucleotides and cysteinyl-leukotrienes, two families of signaling molecules accumulating in brain or heart as a result of hypoxic/traumatic injuries. In subsequent years, evidence of GPR17 key role in oligodendrogenesis and myelination has highlighted it as a "model receptor" for new therapies in demyelinating and neurodegenerative diseases. The apparently contrasting evidence in the literature about the role of GPR17 in promoting or inhibiting myelination can be due to its transient expression in the intermediate stages of differentiation, exerting a pro-differentiating function in early oligodendrocyte precursor cells (OPCs), and an inhibitory role in late stage maturing cells. Meanwhile, several papers extended the initial data on GPR17 pharmacology, highlighting a "promiscuous" behavior of this receptor; indeed, GPR17 is able to respond to other emergency signals like oxysterols or the pro-inflammatory cytokine SDF-1, underlying GPR17 ability to adapt its responses to changes of the surrounding extracellular milieu, including damage conditions. Here, we analyze the available literature on GPR17, in an attempt to summarize its emerging biological roles and pharmacological properties.
    Language English
    Publishing date 2017-08-22
    Publishing country United States
    Document type Journal Article
    ISSN 2214-8019 ; 0065-2598
    ISSN (online) 2214-8019
    ISSN 0065-2598
    DOI 10.1007/5584_2017_92
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Prenatal Stress Impairs Spinal Cord Oligodendrocyte Maturation via BDNF Signaling in the Experimental Autoimmune Encephalomyelitis Model of Multiple Sclerosis.

    Paladini, Maria Serena / Marangon, Davide / Rossetti, Andrea C / Guidi, Alice / Coppolino, Giusy T / Negri, Camilla / Spero, Vittoria / Abbracchio, Maria Pia / Lecca, Davide / Molteni, Raffaella

    Cellular and molecular neurobiology

    2020  Volume 42, Issue 4, Page(s) 1225–1240

    Abstract: One of the most substantial and established environmental risk factors for neurological and psychiatric disorders is stress exposure, whose detrimental consequences hinge on several variables including time. In this regard the gestational period is known ...

    Abstract One of the most substantial and established environmental risk factors for neurological and psychiatric disorders is stress exposure, whose detrimental consequences hinge on several variables including time. In this regard the gestational period is known to present an intrinsic vulnerability to environmental insults and thus stressful events during pregnancy can lead to severe consequences on the offspring's brain development with long-term repercussions throughout adulthood. On this basis, we investigated the long-lasting impact of prenatal stress exposure on the susceptibility to the experimental autoimmune encephalomyelitis (EAE), a well-established murine model of multiple sclerosis. Although stress is considered a triggering factor for this chronic, progressive, autoimmune disease, little is known about the underlying mechanisms. To this end, EAE was induced by immunization with MOG35-55/CFA and pertussis toxin administration in adult female C57BL/6 mice born from control or stressed dams exposed to restraint stress during the last days of gestation. Our results demonstrate that gestational stress induces a marked increase in the severity of EAE symptoms in adulthood. Further, we highlight an altered maturation of oligodendrocytes in the spinal cord of prenatally stressed EAE mice, as indicated by the higher levels of GPR17, a marker of immature oligodendrocyte precursor cells. These behavioral and molecular alterations are paralleled by changes in the expression and signaling of the neurotrophin BDNF, an important mediator of neural plasticity that may contribute to stress-induced impaired remyelination. Since several already marketed drugs are able to modulate BDNF levels, these results pave the way to the possibility of repositioning these drugs in multiple sclerosis.
    MeSH term(s) Animals ; Brain-Derived Neurotrophic Factor/metabolism ; Encephalomyelitis, Autoimmune, Experimental/metabolism ; Female ; Mice ; Mice, Inbred C57BL ; Multiple Sclerosis/metabolism ; Nerve Tissue Proteins/metabolism ; Oligodendroglia/metabolism ; Receptors, G-Protein-Coupled/metabolism ; Spinal Cord/metabolism
    Chemical Substances Bdnf protein, mouse ; Brain-Derived Neurotrophic Factor ; GPR17 protein, human ; GPR17 protein, mouse ; Nerve Tissue Proteins ; Receptors, G-Protein-Coupled
    Language English
    Publishing date 2020-12-01
    Publishing country United States
    Document type Journal Article
    ZDB-ID 283404-2
    ISSN 1573-6830 ; 0272-4340
    ISSN (online) 1573-6830
    ISSN 0272-4340
    DOI 10.1007/s10571-020-01014-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 1727: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (1.OG)
    ab Jg. 2022: Lesesaal (EG)

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  3. Article ; Online: MiR-125a-3p timely inhibits oligodendroglial maturation and is pathologically up-regulated in human multiple sclerosis.

    Lecca, Davide / Marangon, Davide / Coppolino, Giusy T / Méndez, Aida Menéndez / Finardi, Annamaria / Costa, Gloria Dalla / Martinelli, Vittorio / Furlan, Roberto / Abbracchio, Maria P

    Scientific reports

    2016  Volume 6, Page(s) 34503

    Abstract: In the mature central nervous system (CNS), oligodendrocytes provide support and insulation to axons thanks to the production of a myelin sheath. During their maturation to myelinating cells, oligodendroglial precursors (OPCs) follow a very precise ... ...

    Abstract In the mature central nervous system (CNS), oligodendrocytes provide support and insulation to axons thanks to the production of a myelin sheath. During their maturation to myelinating cells, oligodendroglial precursors (OPCs) follow a very precise differentiation program, which is finely orchestrated by transcription factors, epigenetic factors and microRNAs (miRNAs), a class of small non-coding RNAs involved in post-transcriptional regulation. Any alterations in this program can potentially contribute to dysregulated myelination, impaired remyelination and neurodegenerative conditions, as it happens in multiple sclerosis (MS). Here, we identify miR-125a-3p, a developmentally regulated miRNA, as a new actor of oligodendroglial maturation, that, in the mammalian CNS regulates the expression of myelin genes by simultaneously acting on several of its already validated targets. In cultured OPCs, over-expression of miR-125a-3p by mimic treatment impairs while its inhibition with an antago-miR stimulates oligodendroglial maturation. Moreover, we show that miR-125a-3p levels are abnormally high in the cerebrospinal fluid of MS patients bearing active demyelinating lesions, suggesting that its pathological upregulation may contribute to MS development, at least in part by blockade of OPC differentiation leading to impaired repair of demyelinated lesions.
    Language English
    Publishing date 2016-10-04
    Publishing country England
    Document type Journal Article
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/srep34503
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Differential local tissue permissiveness influences the final fate of GPR17-expressing oligodendrocyte precursors in two distinct models of demyelination.

    Coppolino, Giusy T / Marangon, Davide / Negri, Camilla / Menichetti, Gianluca / Fumagalli, Marta / Gelosa, Paolo / Dimou, Leda / Furlan, Roberto / Lecca, Davide / Abbracchio, Maria P

    Glia

    2018  Volume 66, Issue 5, Page(s) 1118–1130

    Abstract: Promoting remyelination is recognized as a novel strategy to foster repair in neurodegenerative demyelinating diseases, such as multiple sclerosis. In this respect, the receptor GPR17, recently emerged as a new target for remyelination, is expressed by ... ...

    Abstract Promoting remyelination is recognized as a novel strategy to foster repair in neurodegenerative demyelinating diseases, such as multiple sclerosis. In this respect, the receptor GPR17, recently emerged as a new target for remyelination, is expressed by early oligodendrocyte precursors (OPCs) and after a certain differentiation stage it has to be downregulated to allow progression to mature myelinating oligodendrocytes. Here, we took advantage of the first inducible GPR17 reporter mouse line (GPR17-iCreER
    MeSH term(s) Animals ; Cuprizone ; Demyelinating Diseases/metabolism ; Demyelinating Diseases/pathology ; Disease Models, Animal ; Female ; Green Fluorescent Proteins/genetics ; Green Fluorescent Proteins/metabolism ; Male ; Mice, Inbred C57BL ; Mice, Transgenic ; Myelin-Oligodendrocyte Glycoprotein ; Nerve Tissue Proteins/metabolism ; Oligodendrocyte Precursor Cells/metabolism ; Oligodendrocyte Precursor Cells/pathology ; Peptide Fragments ; Receptors, G-Protein-Coupled/metabolism ; Remyelination/physiology ; Spinal Cord/metabolism ; Spinal Cord/pathology
    Chemical Substances GPR17 protein, mouse ; Myelin-Oligodendrocyte Glycoprotein ; Nerve Tissue Proteins ; Peptide Fragments ; Receptors, G-Protein-Coupled ; enhanced green fluorescent protein ; myelin oligodendrocyte glycoprotein (35-55) ; Green Fluorescent Proteins (147336-22-9) ; Cuprizone (5N16U7E0AO)
    Language English
    Publishing date 2018-02-09
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 639414-0
    ISSN 1098-1136 ; 0894-1491
    ISSN (online) 1098-1136
    ISSN 0894-1491
    DOI 10.1002/glia.23305
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2345: Show issues Location:
    Je nach Verfügbarkeit (siehe Angabe bei Bestand)
    bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular
    Jg. 1995 - 2021: Lesesall (2.OG)
    ab Jg. 2022: Lesesaal (EG)

    Order via subito

    This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

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