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Tytuł pozycji:

Astrocytes from cortex and striatum show differential responses to mitochondrial toxin and BDNF: implications for protection of striatal neurons expressing mutant huntingtin.

Tytuł:
Astrocytes from cortex and striatum show differential responses to mitochondrial toxin and BDNF: implications for protection of striatal neurons expressing mutant huntingtin.
Autorzy:
Saba J; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
López Couselo F; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Turati J; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Carniglia L; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Durand D; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
de Laurentiis A; Centro de Estudios Farmacológicos y Botánicos (CEFYBO). UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Lasaga M; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina.
Caruso C; Instituto de Investigaciones Biomédicas (INBIOMED), UBA-CONICET, Paraguay 2155, Facultad de Medicina, Universidad de Buenos Aires, Buenos Aires, Argentina. .
Źródło:
Journal of neuroinflammation [J Neuroinflammation] 2020 Oct 06; Vol. 17 (1), pp. 290. Date of Electronic Publication: 2020 Oct 06.
Typ publikacji:
Journal Article
Język:
English
Imprint Name(s):
Original Publication: [London] : BioMed Central, c2004-
MeSH Terms:
Astrocytes/*metabolism
Brain-Derived Neurotrophic Factor/*toxicity
Cerebral Cortex/*metabolism
Corpus Striatum/*metabolism
Huntingtin Protein/*biosynthesis
Nitro Compounds/*toxicity
Propionates/*toxicity
Animals ; Animals, Newborn ; Astrocytes/drug effects ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Cerebral Cortex/drug effects ; Corpus Striatum/drug effects ; Female ; Gene Expression ; Humans ; Huntingtin Protein/genetics ; Male ; Mitochondria/drug effects ; Mitochondria/metabolism ; Mutation/drug effects ; Mutation/physiology ; Neurons/drug effects ; Neurons/metabolism ; Neuroprotection/drug effects ; Neuroprotection/physiology ; Rats ; Rats, Wistar
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Grant Information:
UBACYT20020130200058BA Secretaria de Ciencia y Tecnica, Universidad de Buenos Aires; PICT 2015 1367 Fondo para la Investigación Científica y Tecnológica; 2018 Fundacion Lorena Scarafiocca
Contributed Indexing:
Keywords: 3-Nitropropionic acid; Astrocyte-conditioned medium; BDNF; Cortical astrocytes; Glutamate transporters; Huntington’s disease; ST14A-Q120 striatal neurons; Striatal astrocytes; TGF-β; TNF-α
Substance Nomenclature:
0 (Bdnf protein, rat)
0 (Brain-Derived Neurotrophic Factor)
0 (HTT protein, human)
0 (Huntingtin Protein)
0 (Nitro Compounds)
0 (Propionates)
QY4L0FOX0D (3-nitropropionic acid)
Entry Date(s):
Date Created: 20201007 Date Completed: 20210729 Latest Revision: 20210729
Update Code:
20240105
PubMed Central ID:
PMC7542133
DOI:
10.1186/s12974-020-01965-4
PMID:
33023623
Czasopismo naukowe
Background: Evidence shows significant heterogeneity in astrocyte gene expression and function. We previously demonstrated that brain-derived neurotrophic factor (BDNF) exerts protective effects on whole brain primary cultured rat astrocytes treated with 3-nitropropionic acid (3NP), a mitochondrial toxin widely used as an in vitro model of Huntington's disease (HD). Therefore, we now investigated 3NP and BDNF effects on astrocytes from two areas involved in HD: the striatum and the entire cortex, and their involvement in neuron survival.
Methods: We prepared primary cultured rat cortical or striatal astrocytes and treated them with BDNF and/or 3NP for 24 h. In these cells, we assessed expression of astrocyte markers, BDNF receptor, and glutamate transporters, and cytokine release. We prepared astrocyte-conditioned medium (ACM) from cortical and striatal astrocytes and tested its effect on a cellular model of HD.
Results: BDNF protected astrocytes from 3NP-induced death, increased expression of its own receptor, and activation of ERK in both cortical and striatal astrocytes. However, BDNF modulated glutamate transporter expression differently by increasing GLT1 and GLAST expression in cortical astrocytes but only GLT1 expression in striatal astrocytes. Striatal astrocytes released higher amounts of tumor necrosis factor-α than cortical astrocytes in response to 3NP but BDNF decreased this effect in both populations. 3NP decreased transforming growth factor-β release only in cortical astrocytes, whereas BDNF treatment increased its release only in striatal astrocytes. Finally, we evaluated ACM effect on a cellular model of HD: the rat striatal neuron cell line ST14A expressing mutant human huntingtin (Q120) or in ST14A cells expressing normal human huntingtin (Q15). Neither striatal nor cortical ACM modified the viability of Q15 cells. Only ACM from striatal astrocytes treated with BDNF and ACM from 3NP + BDNF-treated striatal astrocytes protected Q120 cells, whereas ACM from cortical astrocytes did not.
Conclusions: Data suggest that cortical and striatal astrocytes respond differently to mitochondrial toxin 3NP and BDNF. Moreover, striatal astrocytes secrete soluble neuroprotective factors in response to BDNF that selectively protect neurons expressing mutant huntingtin implicating that BDNF modulation of striatal astrocyte function has therapeutic potential against neurodegeneration.
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