Home > Publications Database > Neuron-specific proteasome activation exerts cell non-autonomous protection against amyloid-beta (Aβ) proteotoxicity in Caenorhabditis elegans. > print

001     259961
005     20231004134700.0
024 7 _ |a 10.1016/j.redox.2023.102817
|2 doi
024 7 _ |a pmid:37473700
|2 pmid
024 7 _ |a pmc:PMC10404562
|2 pmc
024 7 _ |a altmetric:151772439
|2 altmetric
037 _ _ |a DZNE-2023-00814
041 _ _ |a English
082 _ _ |a 570
100 1 _ |a Panagiotidou, Eleni
|b 0
245 _ _ |a Neuron-specific proteasome activation exerts cell non-autonomous protection against amyloid-beta (Aβ) proteotoxicity in Caenorhabditis elegans.
260 _ _ |a Amsterdam [u.a.]
|c 2023
|b Elsevier
336 7 _ |a article
|2 DRIVER
336 7 _ |a Output Types/Journal article
|2 DataCite
336 7 _ |a Journal Article
|b journal
|m journal
|0 PUB:(DE-HGF)16
|s 1694700407_30856
|2 PUB:(DE-HGF)
336 7 _ |a ARTICLE
|2 BibTeX
336 7 _ |a JOURNAL_ARTICLE
|2 ORCID
336 7 _ |a Journal Article
|0 0
|2 EndNote
520 _ _ |a Proteostasis reinforcement is a promising approach in the design of therapeutic interventions against proteinopathies, including Alzheimer's disease. Understanding how and which parts of the proteostasis network should be enhanced is crucial in developing efficient therapeutic strategies. The ability of specific tissues to induce proteostatic responses in distal ones (cell non-autonomous regulation of proteostasis) is attracting interest. Although the proteasome is a major protein degradation node, nothing is known on its cell non-autonomous regulation. We show that proteasome activation in the nervous system can enhance the proteasome activity in the muscle of Caenorhabditis elegans. Mechanistically, this communication depends on Small Clear Vesicles, with glutamate as one of the neurotransmitters required for the distal regulation. More importantly, we demonstrate that this cell non-autonomous proteasome activation is translated into efficient prevention of amyloid-beta (Αβ)-mediated proteotoxic effects in the muscle of C. elegans but notably not to resistance against oxidative stress. Our in vivo data establish a mechanistic link between neuronal proteasome reinforcement and decreased Aβ proteotoxicity in the muscle. The identified distal communication may have serious implications in the design of therapeutic strategies based on tissue-specific proteasome manipulation.
536 _ _ |a 351 - Brain Function (POF4-351)
|0 G:(DE-HGF)POF4-351
|c POF4-351
|f POF IV
|x 0
588 _ _ |a Dataset connected to CrossRef, PubMed, , Journals: pub.dzne.de
650 _ 7 |a C. elegans
|2 Other
650 _ 7 |a Cell non-autonomous regulation
|2 Other
650 _ 7 |a Proteasome
|2 Other
650 _ 7 |a Proteinopathies
|2 Other
650 _ 7 |a Proteostasis
|2 Other
650 _ 7 |a Proteasome Endopeptidase Complex
|0 EC 3.4.25.1
|2 NLM Chemicals
650 _ 7 |a Caenorhabditis elegans Proteins
|2 NLM Chemicals
650 _ 7 |a Amyloid beta-Peptides
|2 NLM Chemicals
650 _ 2 |a Animals
|2 MeSH
650 _ 2 |a Caenorhabditis elegans: genetics
|2 MeSH
650 _ 2 |a Caenorhabditis elegans: metabolism
|2 MeSH
650 _ 2 |a Proteasome Endopeptidase Complex: metabolism
|2 MeSH
650 _ 2 |a Caenorhabditis elegans Proteins: genetics
|2 MeSH
650 _ 2 |a Caenorhabditis elegans Proteins: metabolism
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: toxicity
|2 MeSH
650 _ 2 |a Amyloid beta-Peptides: metabolism
|2 MeSH
650 _ 2 |a Neurons: metabolism
|2 MeSH
700 1 _ |a Gioran, Anna
|b 1
700 1 _ |a Bano, Daniele
|0 P:(DE-2719)2158358
|b 2
|u dzne
700 1 _ |a Chondrogianni, Niki
|b 3
773 _ _ |a 10.1016/j.redox.2023.102817
|g Vol. 65, p. 102817 -
|0 PERI:(DE-600)2701011-9
|p 102817
|t Redox Biology
|v 65
|y 2023
|x 2213-2317
856 4 _ |y OpenAccess
|u https://pub.dzne.de/record/259961/files/DZNE-2023-00814.pdf
856 4 _ |y OpenAccess
|x pdfa
|u https://pub.dzne.de/record/259961/files/DZNE-2023-00814.pdf?subformat=pdfa
909 C O |o oai:pub.dzne.de:259961
|p openaire
|p open_access
|p VDB
|p driver
|p dnbdelivery
910 1 _ |a Deutsches Zentrum für Neurodegenerative Erkrankungen
|0 I:(DE-588)1065079516
|k DZNE
|b 2
|6 P:(DE-2719)2158358
913 1 _ |a DE-HGF
|b Gesundheit
|l Neurodegenerative Diseases
|1 G:(DE-HGF)POF4-350
|0 G:(DE-HGF)POF4-351
|3 G:(DE-HGF)POF4
|2 G:(DE-HGF)POF4-300
|4 G:(DE-HGF)POF
|v Brain Function
|x 0
914 1 _ |y 2023
915 _ _ |a OpenAccess
|0 StatID:(DE-HGF)0510
|2 StatID
915 _ _ |a Creative Commons Attribution-NonCommercial-NoDerivs CC BY-NC-ND 4.0
|0 LIC:(DE-HGF)CCBYNCND4
|2 HGFVOC
915 _ _ |a JCR
|0 StatID:(DE-HGF)0100
|2 StatID
|b REDOX BIOL : 2022
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0200
|2 StatID
|b SCOPUS
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0300
|2 StatID
|b Medline
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0320
|2 StatID
|b PubMed Central
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0501
|2 StatID
|b DOAJ Seal
|d 2023-06-05T07:04:07Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0500
|2 StatID
|b DOAJ
|d 2023-06-05T07:04:07Z
915 _ _ |a Peer Review
|0 StatID:(DE-HGF)0030
|2 StatID
|b DOAJ : Anonymous peer review
|d 2023-06-05T07:04:07Z
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0199
|2 StatID
|b Clarivate Analytics Master Journal List
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)1050
|2 StatID
|b BIOSIS Previews
|d 2023-08-22
915 _ _ |a DBCoverage
|0 StatID:(DE-HGF)0150
|2 StatID
|b Web of Science Core Collection
|d 2023-08-22
915 _ _ |a IF >= 10
|0 StatID:(DE-HGF)9910
|2 StatID
|b REDOX BIOL : 2022
|d 2023-08-22
920 1 _ |0 I:(DE-2719)1013003
|k AG Bano
|l Aging and Neurodegeneration
|x 0
980 _ _ |a journal
980 _ _ |a VDB
980 _ _ |a UNRESTRICTED
980 _ _ |a I:(DE-2719)1013003
980 1 _ |a FullTexts

LibraryCollectionCLSMajorCLSMinorLanguageAuthor
Marc 21