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  1. AU="Thomaz, Natalie K"
  2. AU="Ahmed, Mostafa S."
  3. AU="Im, Kate"
  4. AU="Ben Mustapha, Nadia"
  5. AU="Yokoyama, Yukihiro"
  6. AU="Zhu, Yu Peng"
  7. AU="Rbia, Nadia"
  8. AU="Wile, Rachel K"
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  10. AU="Tarantino, Lisa M."
  11. AU="Desidério Favarato"
  12. AU=Becker Stefan
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  14. AU="Ounajim, Amine"
  15. AU=Clothier Hazel J
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  20. AU="Taylor, Maureen E"
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  31. AU=Keller Ray
  32. AU="Gopas, Jacob"
  33. AU="Berthelson, P R"
  34. AU="Rivera-Torres, Juan J"
  35. AU="Henriquez, Javier"
  36. AU="Adele N Burgess"
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  1. Article ; Online: Age-dependent effects of resveratrol in hypothalamic astrocyte cultures.

    Leite Santos, Camila / K Vizuete, Adriana Fernanda / Becker Weber, Fernanda / Thomaz, Natalie K / Bobermin, Larissa Daniele / Gonçalves, Carlos-Alberto / Quincozes-Santos, André

    Neuroreport

    2023  Volume 34, Issue 8, Page(s) 419–425

    Abstract: Objectives: The hypothalamus plays critical roles in maintaining brain homeostasis and increasing evidence has highlighted astrocytes orchestrating several of hypothalamic functions. However, it remains unclear how hypothalamic astrocytes participate in ...

    Abstract Objectives: The hypothalamus plays critical roles in maintaining brain homeostasis and increasing evidence has highlighted astrocytes orchestrating several of hypothalamic functions. However, it remains unclear how hypothalamic astrocytes participate in neurochemical mechanisms associated with aging process, as well as whether these cells can be a target for antiaging strategies. In this sense, the aim of this study is to evaluate the age-dependent effects of resveratrol, a well-characterized neuroprotective compound, in primary astrocyte cultures derived from the hypothalamus of newborn, adult, and aged rats.
    Methods: Male Wistar rats (2, 90, 180, and 365 days old) were used in this study. Cultured astrocytes from different ages were treated with 10 and 100 μM resveratrol and cellular viability, metabolic activity, astrocyte morphology, release of glial cell line-derived neurotrophic factor (GDNF), transforming growth factor β (TGF-β), tumor necrosis factor α (TNF-α), interleukins (IL-1β, IL-6, and IL-10), as well as the protein levels of Nrf2 and HO-1 were evaluated.
    Results: In vitro astrocytes derived from neonatal, adults, and aged animals changed metabolic activity and the release of trophic factors (GDNF and TGF-β), as well as the inflammatory mediators (TNF-α, IL-1β, IL-6, and IL-10). Resveratrol prevented these alterations. In addition, resveratrol changed the immunocontent of Nrf2 and HO-1. The results indicated that the effects of resveratrol seem to have a dose- and age-associated glioprotective role.
    Conclusion: These findings demonstrate for the first time that resveratrol prevents the age-dependent underlying functional reprogramming of in vitro hypothalamic astrocytes, reinforcing its antiaging activity, and consequently, its glioprotective role.
    MeSH term(s) Rats ; Animals ; Male ; Resveratrol/pharmacology ; Astrocytes/metabolism ; Rats, Wistar ; Interleukin-10/pharmacology ; Glial Cell Line-Derived Neurotrophic Factor/metabolism ; Glial Cell Line-Derived Neurotrophic Factor/pharmacology ; Tumor Necrosis Factor-alpha/metabolism ; NF-E2-Related Factor 2/metabolism ; Interleukin-6/metabolism ; Hypothalamus/metabolism ; Transforming Growth Factor beta/metabolism ; Cells, Cultured
    Chemical Substances Resveratrol (Q369O8926L) ; Interleukin-10 (130068-27-8) ; Glial Cell Line-Derived Neurotrophic Factor ; Tumor Necrosis Factor-alpha ; NF-E2-Related Factor 2 ; Interleukin-6 ; Transforming Growth Factor beta
    Language English
    Publishing date 2023-04-25
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1049746-8
    ISSN 1473-558X ; 0959-4965
    ISSN (online) 1473-558X
    ISSN 0959-4965
    DOI 10.1097/WNR.0000000000001906
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 3118: 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)

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  2. Article ; Online: Glioprotective Effects of Resveratrol Against BMAA-Induced Astroglial Dysfunctions.

    Dias, Filipe Renato Pereira / de Souza Almeida, Rômulo Rodrigo / Sovrani, Vanessa / Thomaz, Natalie K / Gonçalves, Carlos-Alberto / Quincozes-Santos, André / Bobermin, Larissa Daniele

    Neurotoxicity research

    2022  Volume 40, Issue 2, Page(s) 530–541

    Abstract: Astroglial cells play important roles in maintaining central nervous system (CNS) homeostasis. The neurotoxin β-N-methylamino-L-alanine (BMAA) has usually been associated with neurodegeneration due to its toxic effects on neurons. However, little is ... ...

    Abstract Astroglial cells play important roles in maintaining central nervous system (CNS) homeostasis. The neurotoxin β-N-methylamino-L-alanine (BMAA) has usually been associated with neurodegeneration due to its toxic effects on neurons. However, little is known about the effects of BMAA on astroglial cells. Resveratrol, a natural polyphenol, represents a potential protective strategy against brain injuries. In the present study, we sought to investigate BMAA-induced astroglial dysfunctions and the glioprotective roles of resveratrol. BMAA did not impair astroglial cellular viability, but increased glutamate uptake, glutamate metabolism into glutamine, and reactive oxygen species production, while decreased glutathione (GSH) and superoxide dismutase (SOD)-based antioxidant defenses and triggers an inflammatory response. In contrast, resveratrol was able to prevent most of these BMAA-induced functional changes in astroglial cells. Moreover, both BMAA and resveratrol modulated the gene expression of molecular pathways associated with glutamate metabolism, redox homeostasis, and inflammatory response, which characterize their roles on astroglial functions. In this regard, BMAA downregulated adenosine receptors, peroxisome proliferator-activated receptor-gamma coactivator 1-alpha (PGC-1α), phosphoinositide-3-kinase (PI3K), and Akt, while resveratrol prevented these effects and upregulated nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1). Our study, for the first time, demonstrates that BMAA directly impacts key astroglial functions, contributing to elucidating the cellular and molecular mechanisms of this toxin in the CNS. In addition, we reinforce the glioprotective effects of resveratrol against BMAA-induced astroglial dysfunctions.
    MeSH term(s) Antioxidants/metabolism ; Antioxidants/pharmacology ; Astrocytes ; Glutamic Acid/metabolism ; Resveratrol/pharmacology ; Signal Transduction
    Chemical Substances Antioxidants ; Glutamic Acid (3KX376GY7L) ; Resveratrol (Q369O8926L)
    Language English
    Publishing date 2022-03-23
    Publishing country United States
    Document type Journal Article
    ZDB-ID 2036826-4
    ISSN 1476-3524 ; 1029-8428
    ISSN (online) 1476-3524
    ISSN 1029-8428
    DOI 10.1007/s12640-022-00492-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 5749: 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)

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  3. Article ; Online: The role of glial cells in Zika virus-induced neurodegeneration.

    Quincozes-Santos, André / Bobermin, Larissa Daniele / Costa, Naithan Ludian Fernandes / Thomaz, Natalie K / Almeida, Rômulo Rodrigo de Souza / Beys-da-Silva, Walter O / Santi, Lucélia / Rosa, Rafael L / Capra, Daniela / Coelho-Aguiar, Juliana M / DosSantos, Marcos Fabio / Heringer, Manoela / Cirne-Lima, Elizabeth O / Guimarães, Jorge Almeida / Schuler-Faccini, Lavínia / Gonçalves, Carlos-Alberto / Moura-Neto, Vivaldo / Souza, Diogo Onofre

    Glia

    2023  Volume 71, Issue 8, Page(s) 1791–1803

    Abstract: Zika virus (ZIKV) is a strongly neurotropic flavivirus whose infection has been associated with microcephaly in neonates. However, clinical and experimental evidence indicate that ZIKV also affects the adult nervous system. In this regard, in vitro and ... ...

    Abstract Zika virus (ZIKV) is a strongly neurotropic flavivirus whose infection has been associated with microcephaly in neonates. However, clinical and experimental evidence indicate that ZIKV also affects the adult nervous system. In this regard, in vitro and in vivo studies have shown the ability of ZIKV to infect glial cells. In the central nervous system (CNS), glial cells are represented by astrocytes, microglia, and oligodendrocytes. In contrast, the peripheral nervous system (PNS) constitutes a highly heterogeneous group of cells (Schwann cells, satellite glial cells, and enteric glial cells) spread through the body. These cells are critical in both physiological and pathological conditions; as such, ZIKV-induced glial dysfunctions can be associated with the development and progression of neurological complications, including those related to the adult and aging brain. This review will address the effects of ZIKV infection on CNS and PNS glial cells, focusing on cellular and molecular mechanisms, including changes in the inflammatory response, oxidative stress, mitochondrial dysfunction, Ca
    MeSH term(s) Humans ; Zika Virus/physiology ; Zika Virus Infection/complications ; Zika Virus Infection/drug therapy ; Zika Virus Infection/pathology ; Neuroglia/metabolism ; Central Nervous System/metabolism ; Brain/metabolism
    Language English
    Publishing date 2023-03-03
    Publishing country United States
    Document type Journal Article ; Review ; 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.24353
    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)

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  4. Article ; Online: Gliotoxicity and Glioprotection: the Dual Role of Glial Cells.

    Quincozes-Santos, André / Santos, Camila Leite / de Souza Almeida, Rômulo Rodrigo / da Silva, Amanda / Thomaz, Natalie K / Costa, Naithan Ludian Fernandes / Weber, Fernanda Becker / Schmitz, Izaviany / Medeiros, Lara Scopel / Medeiros, Lívia / Dotto, Bethina Segabinazzi / Dias, Filipe Renato Pereira / Sovrani, Vanessa / Bobermin, Larissa Daniele

    Molecular neurobiology

    2021  Volume 58, Issue 12, Page(s) 6577–6592

    Abstract: Glial cells (astrocytes, oligodendrocytes and microglia) are critical for the central nervous system (CNS) in both physiological and pathological conditions. With this in mind, several studies have indicated that glial cells play key roles in the ... ...

    Abstract Glial cells (astrocytes, oligodendrocytes and microglia) are critical for the central nervous system (CNS) in both physiological and pathological conditions. With this in mind, several studies have indicated that glial cells play key roles in the development and progression of CNS diseases. In this sense, gliotoxicity can be referred as the cellular, molecular, and neurochemical changes that can mediate toxic effects or ultimately lead to impairment of the ability of glial cells to protect neurons and/or other glial cells. On the other hand, glioprotection is associated with specific responses of glial cells, by which they can protect themselves as well as neurons, resulting in an overall improvement of the CNS functioning. In addition, gliotoxic events, including metabolic stresses, inflammation, excitotoxicity, and oxidative stress, as well as their related mechanisms, are strongly associated with the pathogenesis of neurological, psychiatric and infectious diseases. However, glioprotective molecules can prevent or improve these glial dysfunctions, representing glial cells-targeting therapies. Therefore, this review will provide a brief summary of types and functions of glial cells and point out cellular and molecular mechanisms associated with gliotoxicity and glioprotection, potential glioprotective molecules and their mechanisms, as well as gliotherapy. In summary, we expect to address the relevance of gliotoxicity and glioprotection in the CNS homeostasis and diseases.
    MeSH term(s) Animals ; Brain/drug effects ; Brain/metabolism ; Neuroglia/drug effects ; Neuroglia/metabolism ; Neuroprotective Agents/pharmacology ; Oxidative Stress/drug effects ; Oxidative Stress/physiology
    Chemical Substances Neuroprotective Agents
    Language English
    Publishing date 2021-09-28
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 645020-9
    ISSN 1559-1182 ; 0893-7648
    ISSN (online) 1559-1182
    ISSN 0893-7648
    DOI 10.1007/s12035-021-02574-9
    Database MEDical Literature Analysis and Retrieval System OnLINE

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    In stock of ZB MED Cologne/Königswinter

    Zs.A 2411: 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)

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  5. Article ; Online: Zika virus exposure affects neuron-glia communication in the hippocampal slices of adult rats.

    Bobermin, Larissa Daniele / Quincozes-Santos, André / Santos, Camila Leite / Varela, Ana Paula M / Teixeira, Thais F / Wartchow, Krista Minéia / Lissner, Lílian Juliana / da Silva, Amanda / Thomaz, Natalie K / Santi, Lucélia / Beys-da-Silva, Walter O / Roehe, Paulo M / Sesterheim, Patrícia / Guimarães, Jorge A / Gonçalves, Carlos-Alberto / Souza, Diogo Onofre

    Scientific reports

    2020  Volume 10, Issue 1, Page(s) 21604

    Abstract: Zika virus (ZIKV) infection during pregnancy was associated with microcephaly in neonates, but clinical and experimental evidence indicate that ZIKV also causes neurological complications in adults. However, the changes in neuron-glial communication, ... ...

    Abstract Zika virus (ZIKV) infection during pregnancy was associated with microcephaly in neonates, but clinical and experimental evidence indicate that ZIKV also causes neurological complications in adults. However, the changes in neuron-glial communication, which is essential for brain homeostasis, are still unknown. Here, we report that hippocampal slices from adult rats exposed acutely to ZIKV showed significant cellular alterations regarding to redox homeostasis, inflammatory process, neurotrophic functions and molecular signalling pathways associated with neurons and glial cells. Our findings support the hypothesis that ZIKV is highly neurotropic and its infection readily induces an inflammatory response, characterized by an increased expression and/or release of pro-inflammatory cytokines. We also observed changes in neural parameters, such as adenosine receptor A2a expression, as well as in the release of brain-derived neurotrophic factor and neuron-specific enolase, indicating plasticity synaptic impairment/neuronal damage. In addition, ZIKV induced a glial commitment, with alterations in specific and functional parameters such as aquaporin 4 expression, S100B secretion and glutathione synthesis. ZIKV also induced p21 senescence-associated gene expression, indicating that ZIKV may induce early senescence. Taken together, our results indicate that ZIKV-induced neuroinflammation, involving nuclear factor erythroid 2-related factor 2 (Nrf2) and nuclear factor κB (NFκB) pathways, affects important aspects of neuron-glia communication. Therefore, although ZIKV infection is transient, long-term consequences might be associated with neurological and/or neurodegenerative diseases.
    MeSH term(s) Animals ; Cell Communication ; Female ; Hippocampus/pathology ; Male ; Neuroglia/pathology ; Neurons/pathology ; Pregnancy ; Rats ; Rats, Wistar ; Zika Virus/pathogenicity ; Zika Virus Infection/pathology
    Language English
    Publishing date 2020-12-10
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2615211-3
    ISSN 2045-2322 ; 2045-2322
    ISSN (online) 2045-2322
    ISSN 2045-2322
    DOI 10.1038/s41598-020-78735-y
    Database MEDical Literature Analysis and Retrieval System OnLINE

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