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@ARTICLE{Panagiotidou:259961,
      author       = {Panagiotidou, Eleni and Gioran, Anna and Bano, Daniele and
                      Chondrogianni, Niki},
      title        = {{N}euron-specific proteasome activation exerts cell
                      non-autonomous protection against amyloid-beta ({A}β)
                      proteotoxicity in {C}aenorhabditis elegans.},
      journal      = {Redox Biology},
      volume       = {65},
      issn         = {2213-2317},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-00814},
      pages        = {102817},
      year         = {2023},
      abstract     = {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.},
      keywords     = {Animals / Caenorhabditis elegans: genetics / Caenorhabditis
                      elegans: metabolism / Proteasome Endopeptidase Complex:
                      metabolism / Caenorhabditis elegans Proteins: genetics /
                      Caenorhabditis elegans Proteins: metabolism / Amyloid
                      beta-Peptides: toxicity / Amyloid beta-Peptides: metabolism
                      / Neurons: metabolism / C. elegans (Other) / Cell
                      non-autonomous regulation (Other) / Proteasome (Other) /
                      Proteinopathies (Other) / Proteostasis (Other) / Proteasome
                      Endopeptidase Complex (NLM Chemicals) / Caenorhabditis
                      elegans Proteins (NLM Chemicals) / Amyloid beta-Peptides
                      (NLM Chemicals)},
      cin          = {AG Bano},
      ddc          = {570},
      cid          = {I:(DE-2719)1013003},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37473700},
      pmc          = {pmc:PMC10404562},
      doi          = {10.1016/j.redox.2023.102817},
      url          = {https://pub.dzne.de/record/259961},
}