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Tytuł pozycji:

Dysregulation of prostaglandine E2 and BDNF signaling mediated by estrogenic dysfunction induces primary hippocampal neuronal cell death after single and repeated paraquat treatment.

Tytuł :
Dysregulation of prostaglandine E2 and BDNF signaling mediated by estrogenic dysfunction induces primary hippocampal neuronal cell death after single and repeated paraquat treatment.
Autorzy :
Moyano P; Department of Pharmacology and Toxicology, Veterinary School, Complutense University of Madrid, 28040, Madrid, Spain.
Sanjuan J; Department of Pharmacology and Toxicology, Veterinary School, Complutense University of Madrid, 28040, Madrid, Spain.
García JM; Department of Pharmacology and Toxicology, Veterinary School, Complutense University of Madrid, 28040, Madrid, Spain.
Anadon MJ; Department of Legal Medicine, Psychiatry and Pathology, Medical School, Complutense University of Madrid, 28041, Madrid, Spain.
Naval MV; Department of Pharmacology, Pharmacognosy and Botany, Pharmacy School, Complutense University of Madrid, 28041, Madrid, Spain.
Sola E; Department of Legal Medicine, Psychiatry and Pathology, Medical School, Complutense University of Madrid, 28041, Madrid, Spain.
García J; Department of Pharmacology, Health Sciences School, Alfonso X University, 28691, Madrid, Spain.
Frejo MT; Department of Pharmacology and Toxicology, Veterinary School, Complutense University of Madrid, 28040, Madrid, Spain.
Pino JD; Department of Pharmacology and Toxicology, Veterinary School, Complutense University of Madrid, 28040, Madrid, Spain. Electronic address: .
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Źródło :
Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association [Food Chem Toxicol] 2020 Oct; Vol. 144, pp. 111611. Date of Electronic Publication: 2020 Jul 30.
Typ publikacji :
Journal Article
Język :
English
Imprint Name(s) :
Publication: Exeter : Elsevier Science Ltd
Original Publication: Oxford ; New York : Pergamon Press, c1982-
Contributed Indexing :
Keywords: Aβ and Tau proteins; BDNF; Cell death; ER; Hippocampal neurons; Oxidative stress; PGE2; Paraquat
Entry Date(s) :
Date Created: 20200802 Latest Revision: 20200915
Update Code :
20201218
DOI :
10.1016/j.fct.2020.111611
PMID :
32738378
Czasopismo naukowe
Paraquat (PQ) produces hippocampal neuronal cell death and cognitive dysfunctions after unique and continued exposure, but the mechanisms are not understood. Primary hippocampal wildtype or βAPP-Tau silenced cells were co-treated with PQ with or without E2, N-acetylcysteine (NAC), NS-398 (cyclooxygenase-2 inhibitor), MF63 (PGES-1 inhibitor) and/or recombinant brain-derived neurotrophic factor (BDNF) during one- and fourteen-days to studied PQ effect on prostaglandin E2 (PGE2) and BDNF signaling and their involvement in hyperphosphorylated Tau (pTau) and amyloid-beta (Aβ) protein formation, and oxidative stress generation, that lead to neuronal cell loss through estrogenic disruption, as a possible mechanism of cognitive dysfunctions produced by PQ. Our results indicate that PQ overexpressed cyclooxygenase-2 that leads to an increase of PGE2 and alters the expression of EP1-3 receptor subtypes. PQ induced also a decrease of proBDNF and mature BDNF levels and altered P75 NTR and tropomyosin receptor kinase B (TrkB) expression. PQ induced PGE2 and BDNF signaling dysfunction, mediated through estrogenic disruption, leading to Aβ and pTau proteins synthesis, oxidative stress generation and finally to cell death. Our research provides relevant information to explain PQ hippocampal neurotoxic effects, indicating a probable explanation of the cognitive dysfunction observed and suggests new therapeutic strategies to protect against PQ toxic effects.
(Copyright © 2020 Elsevier Ltd. All rights reserved.)

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