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@ARTICLE{Boehmerle:140030,
      author       = {Boehmerle, Wolfgang and Huehnchen, Petra and Lee, Sabrina
                      Lin Lin and Harms, Christoph and Endres, Matthias},
      title        = {{TRPV}4 inhibition prevents paclitaxel-induced
                      neurotoxicity in preclinical models.},
      journal      = {Experimental neurology},
      volume       = {306},
      issn         = {0014-4886},
      address      = {Orlando, Fla.},
      publisher    = {Academic Press},
      reportid     = {DZNE-2020-06352},
      pages        = {64-75},
      year         = {2018},
      abstract     = {Paclitaxel is a cytotoxic drug which frequently causes
                      sensory peripheral neuropathy in patients. Increasing
                      evidence suggests that altered intracellular calcium (Ca2+)
                      signals play an important role in the pathogenesis of this
                      condition. In the present study, we examined the interplay
                      between Ca2+ release channels in the endoplasmic reticulum
                      (ER) and Ca2+ permeable channels in the plasma membrane in
                      the context of paclitaxel mediated neurotoxicity. We
                      observed that in small to medium size dorsal root ganglia
                      neurons (DRGN) the inositol-trisphosphate receptor (InsP3R)
                      type 1 was often concentrated in the periphery of cells,
                      which is in contrast to homogenous ER distribution. G
                      protein-coupled designer receptors were used to further
                      elucidate phosphoinositide mediated Ca2+ signaling: This
                      approach showed strong InsP3 mediated Ca2+ signals close to
                      the plasma membrane, which can be amplified by Ca2+ entry
                      through TRPV4 channels. In addition, our results support a
                      physical interaction and partial colocalization of InsP3R1
                      and TRPV4 channels. In the context of paclitaxel-induced
                      neurotoxicity, blocking Ca2+ influx through TRPV4 channels
                      reduced cell death in cultured DRGN. Pretreatment of mice
                      with the pharmacological TRPV4 inhibitor HC067047 prior to
                      paclitaxel injections prevented electrophysiological and
                      behavioral changes associated with paclitaxel-induced
                      neuropathy. In summary, these results underline the
                      relevance of TRPV4 signaling for the pathogenesis of
                      paclitaxel-induced neuropathy and suggest novel preventive
                      strategies.},
      keywords     = {Animals / Antineoplastic Agents, Phytogenic: toxicity /
                      Calcium Channels: drug effects / Calcium Channels:
                      metabolism / Calcium Signaling: drug effects / Cell Death:
                      drug effects / Cell Membrane: drug effects / Cell Membrane:
                      metabolism / Endoplasmic Reticulum: drug effects /
                      Endoplasmic Reticulum: metabolism / Ganglia, Spinal:
                      pathology / Immunohistochemistry / Inositol
                      1,4,5-Trisphosphate Receptors: genetics / Mice, Inbred C57BL
                      / Neurotoxicity Syndromes: pathology / Neurotoxicity
                      Syndromes: prevention $\&$ control / Paclitaxel: toxicity /
                      Rats / Rats, Wistar / TRPV Cation Channels: antagonists $\&$
                      inhibitors / Transfection / Antineoplastic Agents,
                      Phytogenic (NLM Chemicals) / Calcium Channels (NLM
                      Chemicals) / Inositol 1,4,5-Trisphosphate Receptors (NLM
                      Chemicals) / TRPV Cation Channels (NLM Chemicals) / Trpv4
                      protein, mouse (NLM Chemicals) / Trpv4 protein, rat (NLM
                      Chemicals) / Paclitaxel (NLM Chemicals)},
      cin          = {AG Endres},
      ddc          = {610},
      cid          = {I:(DE-2719)1811005},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:29715474},
      doi          = {10.1016/j.expneurol.2018.04.014},
      url          = {https://pub.dzne.de/record/140030},
}