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@ARTICLE{Hingorani:269434,
      author       = {Hingorani, Sonia and Paniagua Soriano, Guillem and Sánchez
                      Huertas, Carlos and Villalba Riquelme, Eva María and López
                      Mocholi, Eric and Martínez Rojas, Beatriz and Alastrué
                      Agudo, Ana and Dupraz, Sebastián and Ferrer Montiel,
                      Antonio Vicente and Moreno Manzano, Victoria},
      title        = {{T}ransplantation of dorsal root ganglia overexpressing the
                      {N}a{C}h{B}ac sodium channel improves locomotion after
                      complete {SCI}},
      journal      = {Molecular therapy},
      volume       = {32},
      number       = {6},
      issn         = {1525-0016},
      address      = {New York, NY},
      publisher    = {Nature Publ. Group},
      reportid     = {DZNE-2024-00531},
      pages        = {1739 - 1759},
      year         = {2024},
      abstract     = {Spinal cord injury (SCI) is a debilitating condition
                      currently lacking treatment. Severe SCI causes the loss of
                      most supraspinal inputs and neuronal activity caudal to the
                      injury, which, coupled with the limited endogenous capacity
                      for spontaneous regeneration, can lead to complete
                      functional loss even in anatomically incomplete lesions. We
                      hypothesized that transplantation of mature dorsal root
                      ganglia (DRGs) genetically modified to express the NaChBac
                      sodium channel could serve as a therapeutic option for
                      functionally complete SCI. We found that NaChBac expression
                      increased the intrinsic excitability of DRG neurons and
                      promoted cell survival and neurotrophic factor secretion in
                      vitro. Transplantation of NaChBac-expressing dissociated
                      DRGs improved voluntary locomotion 7 weeks after injury
                      compared to control groups. Animals transplanted with
                      NaChBac-expressing DRGs also possessed higher
                      tubulin-positive neuronal fiber and myelin preservation,
                      although serotonergic descending fibers remained unaffected.
                      We observed early preservation of the corticospinal tract 14
                      days after injury and transplantation, which was lost 7
                      weeks after injury. Nevertheless, transplantation of
                      NaChBac-expressing DRGs increased the neuronal excitatory
                      input by an increased number of VGLUT2 contacts immediately
                      caudal to the injury. Our work suggests that the
                      transplantation of NaChBac-expressing dissociated DRGs can
                      rescue significant motor function, retaining an excitatory
                      neuronal relay activity immediately caudal to injury.},
      keywords     = {Ganglia, Spinal: metabolism / Animals / Spinal Cord
                      Injuries: metabolism / Spinal Cord Injuries: therapy /
                      Spinal Cord Injuries: genetics / Locomotion / Sodium
                      Channels: metabolism / Sodium Channels: genetics / Rats /
                      Female / Recovery of Function / Disease Models, Animal /
                      Neurons: metabolism / Mice / Gene Expression / Myelin
                      Sheath: metabolism / Cell Survival / dorsal root ganglia
                      (Other) / functional recovery (Other) / inhibitory and
                      excitatory input (Other) / neuronal survival (Other) /
                      neuronal transplantation (Other) / sodium channel (Other) /
                      spinal cord injury (Other) / Sodium Channels (NLM
                      Chemicals)},
      cin          = {AG Bradke},
      ddc          = {610},
      cid          = {I:(DE-2719)1013002},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11184342},
      pubmed       = {pmid:38556794},
      doi          = {10.1016/j.ymthe.2024.03.038},
      url          = {https://pub.dzne.de/record/269434},
}