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@ARTICLE{Ladwig:863072,
      author       = {Ladwig, Anne and Rogall, Rebecca and Hucklenbroich, Jörg
                      and Willuweit, Antje and Schoeneck, Michael and Langen,
                      Karl-Josef and Fink, Gereon R. and Adele Rueger, M. and
                      Schroeter, Michael},
      title        = {{O}steopontin {A}ttenuates {S}econdary {N}eurodegeneration
                      in the {T}halamus after {E}xperimental {S}troke},
      journal      = {Journal of neuroImmune pharmacology},
      volume       = {14},
      number       = {2},
      issn         = {1557-1904},
      address      = {Boston, MA [u.a.]},
      publisher    = {Springer},
      reportid     = {FZJ-2019-03189},
      pages        = {295 - 311},
      year         = {2019},
      abstract     = {Cortical cerebral ischemia elicits neuroinflammation as
                      well as secondary neuronal degeneration in remote areas.
                      Locally distinct and specific secondary neurodegeneration
                      affecting thalamic nuclei connected to cortical areas
                      highlights such processes. Osteopontin (OPN) is a
                      cytokine-like glycoprotein that is excreted in high amounts
                      after cerebral ischemia and exerts various immunomodulatory
                      functions. We here examined putative protective effects of
                      OPN in secondary thalamic degeneration. We subjected male
                      Wistar rats to photothrombosis and subsequently injected OPN
                      or placebo intracerebroventricularly. Immunohistochemical
                      and fluorescence staining was used to detect the extent of
                      neuronal degeneration and microglia activation. Ex vivo
                      autoradiography with radiotracers available for human in
                      vivo PET studies, i.e., cis-4-[18F]Fluor-d-Proline
                      (D-cis-[18F]FPro), and [6-3H]thymidine ([3H]thymidine),
                      confirmed degeneration and proliferation, respectively. We
                      found secondary neurodegeneration in the thalamus
                      characterized by microglial activation and neuronal loss.
                      Neuronal loss was restricted to areas of microglial
                      infiltration. Treatment with OPN significantly decreased
                      neurodegeneration, inflammation and microglial
                      proliferation. Microglia displayed morphological signs of
                      activation without expressing markers of M1 or M2
                      polarization. D-cis-[18F]FPro-uptake mirrored attenuated
                      degeneration in OPN-treated animals. Notably, [3H]thymidine
                      and BrdU-staining revealed increased stem cell proliferation
                      after treatment with OPN. The data suggest that OPN is able
                      to ameliorate secondary neurodegeneration in thalamic
                      nuclei. These effects can be visualized by radiotracers
                      D-cis-[18F]FPro and [3H]thymidine, opening new vistas for
                      translational studies.},
      cin          = {INM-4 / INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-4-20090406 / I:(DE-Juel1)INM-3-20090406},
      pnm          = {573 - Neuroimaging (POF3-573)},
      pid          = {G:(DE-HGF)POF3-573},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30488353},
      UT           = {WOS:000468351800011},
      doi          = {10.1007/s11481-018-9826-1},
      url          = {https://juser.fz-juelich.de/record/863072},
}