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@ARTICLE{Arribas:268530,
      author       = {Arribas, Víctor and Onetti, Yara and Ramiro-Pareta, Marina
                      and Villacampa, Pilar and Beck, Heike and Alberola, Mariona
                      and Esteve-Codina, Anna and Merkel, Angelika and Sperandio,
                      Markus and Martínez-Estrada, Ofelia M and Schmid, Bettina
                      and Montanez, Eloi},
      title        = {{E}ndothelial {TDP}-43 controls sprouting angiogenesis and
                      vascular barrier integrity, and its deletion triggers
                      neuroinflammation.},
      journal      = {JCI insight},
      volume       = {9},
      number       = {5},
      issn         = {2379-3708},
      address      = {Ann Arbor, Michigan},
      publisher    = {JCI Insight},
      reportid     = {DZNE-2024-00271},
      pages        = {e177819},
      year         = {2024},
      abstract     = {TAR DNA-binding protein 43 (TDP-43) is a DNA/RNA-binding
                      protein that regulates gene expression, and its malfunction
                      in neurons has been causally associated with multiple
                      neurodegenerative disorders. Although progress has been made
                      in understanding the functions of TDP-43 in neurons, little
                      is known about its roles in endothelial cells (ECs),
                      angiogenesis, and vascular function. Using inducible
                      EC-specific TDP-43-KO mice, we showed that TDP-43 is
                      required for sprouting angiogenesis, vascular barrier
                      integrity, and blood vessel stability. Postnatal EC-specific
                      deletion of TDP-43 led to retinal hypovascularization due to
                      defects in vessel sprouting associated with reduced EC
                      proliferation and migration. In mature blood vessels, loss
                      of TDP-43 disrupted the blood-brain barrier and triggered
                      vascular degeneration. These vascular defects were
                      associated with an inflammatory response in the CNS with
                      activation of microglia and astrocytes. Mechanistically,
                      deletion of TDP-43 disrupted the fibronectin matrix around
                      sprouting vessels and reduced β-catenin signaling in ECs.
                      Together, our results indicate that TDP-43 is essential for
                      the formation of a stable and mature vasculature.},
      keywords     = {Mice / Animals / Endothelial Cells: metabolism /
                      Neuroinflammatory Diseases / Angiogenesis /
                      Neovascularization, Physiologic: genetics / DNA-Binding
                      Proteins: genetics / DNA-Binding Proteins: metabolism /
                      Angiogenesis (Other) / Endothelial cells (Other) / Vascular
                      biology (Other) / DNA-Binding Proteins (NLM Chemicals)},
      cin          = {AG Schmid},
      ddc          = {610},
      cid          = {I:(DE-2719)1140002},
      pnm          = {352 - Disease Mechanisms (POF4-352)},
      pid          = {G:(DE-HGF)POF4-352},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11143933},
      pubmed       = {pmid:38300714},
      doi          = {10.1172/jci.insight.177819},
      url          = {https://pub.dzne.de/record/268530},
}