% IMPORTANT: The following is UTF-8 encoded.  This means that in the presence
% of non-ASCII characters, it will not work with BibTeX 0.99 or older.
% Instead, you should use an up-to-date BibTeX implementation like “bibtex8” or
% “biber”.

@ARTICLE{Vay:902080,
      author       = {Vay, Sabine Ulrike and Olschewski, Daniel Navin and
                      Petereit, Helena and Lange, Felix and Nazarzadeh, Nilufar
                      and Gross, Elena and Rabenstein, Monika and Blaschke, Stefan
                      Johannes and Fink, Gereon Rudolf and Schroeter, Michael and
                      Rueger, Maria Adele},
      title        = {{O}steopontin regulates proliferation, migration, and
                      survival of astrocytes depending on their activation
                      phenotype},
      journal      = {Journal of neuroscience research},
      volume       = {9},
      number       = {11},
      issn         = {1097-4547},
      address      = {New York, NY [u.a.]},
      publisher    = {Wiley-Liss},
      reportid     = {FZJ-2021-04020},
      pages        = {2822-2843},
      year         = {2021},
      abstract     = {The glycoprotein osteopontin is highly upregulated in
                      central nervous system (CNS) disorders such as ischemic
                      stroke. Osteopontin regulates cell growth, cell adhesion,
                      homeostasis, migration, and survival of various cell types.
                      Accordingly, osteopontin is considered an essential
                      regulator of regeneration and repair in the ischemic milieu.
                      Astrocytes are the most abundant cells in the CNS and play
                      significant roles in health and disease. Astrocytes are
                      involved in homeostasis, promote neuroprotection, and
                      regulate synaptic plasticity. Upon activation, astrocytes
                      may adopt different phenotypes, termed A1 and A2. The direct
                      effects of osteopontin on astrocytes, especially in distinct
                      activation states, are yet unknown. The current study aimed
                      to elucidate the impact of osteopontin on resting and active
                      astrocytes. We established an inflammatory in vitro model of
                      activated (A1) primary astrocytes derived from neonatal
                      wistar rats by exposure to a distinct combination of
                      proinflammatory cytokines. To model ischemic stroke in
                      vitro, astrocytes were subjected to oxygen and glucose
                      deprivation (OGD) in the presence or absence of osteopontin.
                      Osteopontin modulated the activation phenotype by
                      attenuating A1- and restoring A2-marker expression without
                      compromising the active astrocytes’ immunocompetence.
                      Osteopontin promoted the proliferation of active and the
                      migration of resting astrocytes. Following transient OGD,
                      osteopontin mitigated the delayed ongoing death of primary
                      astrocytes, promoting their survival. Data suggest that
                      osteopontin differentially regulates essential functions of
                      resting and active astrocytes and confirm a significant
                      regulatory role of osteopontin in an in vitro ischemia
                      model. Furthermore, the data suggest that osteopontin
                      constitutes a promising target for experimental therapies
                      modulating neuroregeneration and repair.},
      cin          = {INM-3},
      ddc          = {570},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5251},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:34510519},
      UT           = {WOS:000695029500001},
      doi          = {10.1002/jnr.24954},
      url          = {https://juser.fz-juelich.de/record/902080},
}