Tau phosphorylation and neuroinflammatory response to Aβ in
choroid plexus cells

k 2024

Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells

ORVISKÁ, Petra; Parisa EMAMIAREF; Karolína JEŘÁBKOVÁ; Václav BRÁZDA; Alemeh ZAMANI et al.

Základní údaje

Originální název

Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells

Autoři

ORVISKÁ, Petra; Parisa EMAMIAREF; Karolína JEŘÁBKOVÁ; Václav BRÁZDA a Alemeh ZAMANI

Vydání

Morphology 2024, 2024

Další údaje

Jazyk

angličtina

Typ výsledku

Prezentace na konferencích

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Označené pro přenos do RIV

ISBN

978-80-280-0585-6

Příznaky

Mezinárodní význam

Změněno: 11. 9. 2024 11:46, Mgr. Petra Orviská

Anotace

V originále

The pathogenesis of Alzheimer's disease is associated with the accumulation of amyloid-beta peptide and hyperphosphorylated Tau protein, leading to neuronal death. Aβ has been found to interfere with pathways that regulate the phosphorylation of Tau protein, especially in neuroinflammatory response. The blood-cerebrospinal fluid barrier and the choroid plexus play a key role in removing Aβ from the brain and may propagate its toxicity and Tau phosphorylation through neuroinflammatory reactions. The aim of the study was to confirm the relationship between neuroinflammation and increased Tau protein phosphorylation in a rat model cell line of the choroid plexus epithelium. The rat choroid plexus epithelium cell line Z310 was cultivated with Aβ peptide for one and three day timepoints alongside non-treated control. Reverse transcription PCR was used to detect pro-inflammatory cytokines IL1β, IL6, TNFα, and IFNγ, and immunocytochemistry was used to detect p-Tau at the phosphorylation sites T231, S199 and T181. By calculating fold change values of RT-PCR, gene expression changes were observed. By the three day timepoint, a significant rise in expression was evident for most genes, particularly IL6 in the treated group. Notably, IL1β exhibited prominent expression even after just one day of treatment, indicating its rapid response to Aβ exposure. Among the three Tau phosphorylation sites studied, the T231 site exhibited statistically significant changes in response to Aβ treatment upon calculating the corrected total cell fluorescence. It was found that the mRNA expression of pro-inflammatory cytokines IL1β, IL6, TNFα, and IFNγ, as well as p-Tau protein levels increased after Aβ treatment of the Z310 cells, supporting the main hypothesis that neuroinflammation in the choroid plexus epithelium is connected to Tau phosphorylation.

Návaznosti

MUNI/11/JRG/1143/2023, interní kód MU

Název: Junior research group: Choroid Plexus in Diseases

Investor: Masarykova univerzita, Junior research group: Choroid Plexus in Diseases, Juniorní výzkumná skupina

Citovat

ORVISKÁ, Petra; Parisa EMAMIAREF; Karolína JEŘÁBKOVÁ; Václav BRÁZDA a Alemeh ZAMANI. Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells. In Morphology 2024. 2024. ISBN 978-80-280-0585-6.

@proceedings{2431545,
   author = {Orviská, Petra and Emamiaref, Parisa and Jeřábková, Karolína and Brázda, Václav and Zamani, Alemeh},
   booktitle = {Morphology 2024},
   language = {eng},
   isbn = {978-80-280-0585-6},
   title = {Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells},
   url = {https://morphology.med.muni.cz/},
   year = {2024}
}

TY  - CONF
ID  - 2431545
AU  - Orviská, Petra - Emamiaref, Parisa - Jeřábková, Karolína - Brázda, Václav - Zamani, Alemeh
PY  - 2024
TI  - Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells
SN  - 9788028005856
UR  - https://morphology.med.muni.cz/
N2  - The pathogenesis of Alzheimer's disease is associated with the accumulation of amyloid-beta peptide and hyperphosphorylated Tau protein, leading to neuronal death. Aβ has been found to interfere with pathways that regulate the phosphorylation of Tau protein, especially in neuroinflammatory response. The blood-cerebrospinal fluid barrier and the choroid plexus play a key role in removing Aβ from the brain and may propagate its toxicity and Tau phosphorylation through neuroinflammatory reactions. The aim of the study was to confirm the relationship between neuroinflammation and increased Tau protein phosphorylation in a rat model cell line of the choroid plexus epithelium. The rat choroid plexus epithelium cell line Z310 was cultivated with Aβ peptide for one and three day timepoints alongside non-treated control. Reverse transcription PCR was used to detect pro-inflammatory cytokines IL1β, IL6, TNFα, and IFNγ, and immunocytochemistry was used to detect p-Tau at the phosphorylation sites T231, S199 and T181. By calculating fold change values of RT-PCR, gene expression changes were observed. By the three day timepoint, a significant rise in expression was evident for most genes, particularly IL6 in the treated group. Notably, IL1β exhibited prominent expression even after just one day of treatment, indicating its rapid response to Aβ exposure. Among the three Tau phosphorylation sites studied, the T231 site exhibited statistically significant changes in response to Aβ treatment upon calculating the corrected total cell fluorescence. It was found that the mRNA expression of pro-inflammatory cytokines IL1β, IL6, TNFα, and IFNγ, as well as p-Tau protein levels increased after Aβ treatment of the Z310 cells, supporting the main hypothesis that neuroinflammation in the choroid plexus epithelium is connected to Tau phosphorylation.
ER  -

ORVISKÁ, Petra; Parisa EMAMIAREF; Karolína JEŘÁBKOVÁ; Václav BRÁZDA a Alemeh ZAMANI. Tau phosphorylation and neuroinflammatory response to Aβ in choroid plexus cells. In \textit{Morphology 2024}. 2024. ISBN~978-80-280-0585-6.

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