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@ARTICLE{Olschewski:1028966,
      author       = {Olschewski, Daniel Navin and Nazarzadeh, Nilufar and Lange,
                      Felix and Koenig, Anna Maria and Kulka, Christina and
                      Abraham, Jella-Andrea and Blaschke, Stefan Johannes and
                      Merkel, Rudolf and Hoffmann, Bernd and Fink, Gereon Rudolf
                      and Schroeter, Michael and Rueger, Maria Adele and Vay,
                      Sabine Ulrike},
      title        = {{T}he angiotensin {II} receptors type 1 and 2 modulate
                      astrocytes and their crosstalk with microglia and neurons in
                      an in vitro model of ischemic stroke},
      journal      = {BMC neuroscience},
      volume       = {25},
      number       = {1},
      issn         = {1471-2202},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {FZJ-2024-04902},
      pages        = {29},
      year         = {2024},
      abstract     = {AbstractBackground Astrocytes are the most abundant cell
                      type of the central nervous system and are
                      fundamentallyinvolved in homeostasis, neuroprotection, and
                      synaptic plasticity. This regulatory function of astrocytes
                      on theirneighboring cells in the healthy brain is subject of
                      current research. In the ischemic brain we assume disease
                      specificdifferences in astrocytic acting. The
                      renin–angiotensin–aldosterone system regulates arterial
                      blood pressurethrough endothelial cells and perivascular
                      musculature. Moreover, astrocytes express angiotensin II
                      type 1 and 2receptors. However, their role in astrocytic
                      function has not yet been fully elucidated. We hypothesized
                      that the angiotensinII receptors impact astrocyte function
                      as revealed in an in vitro system mimicking cerebral
                      ischemia.Astrocytes derived from neonatal wistar rats were
                      exposed to telmisartan (angiotensin II type 1
                      receptor-blocker)or PD123319 (angiotensin II type 2
                      receptor-blocker) under normal conditions (control) or
                      deprivation from oxygenand glucose. Conditioned medium (CM)
                      of astrocytes was harvested to elucidate astrocyte-mediated
                      indirect effectson microglia and cortical neurons.Result The
                      blockade of angiotensin II type 1 receptor by telmisartan
                      increased the survival of astrocytes duringischemic
                      conditions in vitro without affecting their proliferation
                      rate or disturbing their expression of S100A10,a marker of
                      activation. The inhibition of the angiotensin II type 2
                      receptor pathway by PD123319 resultedin both increased
                      expression of S100A10 and proliferation rate. The CM of
                      telmisartan-treated astrocytes reducedthe expression of
                      pro-inflammatory mediators with simultaneous increase of
                      anti-inflammatory markers in microglia.Increased neuronal
                      activity was observed after treatment of neurons with CM of
                      telmisartan- as well as PD123319-stimulated
                      astrocytes.Conclusion Data show that angiotensin II
                      receptors have functional relevance for astrocytes that
                      differs in healthyand ischemic conditions and effects
                      surrounding microglia and neuronal activity via secretory
                      signals. Above that, this},
      cin          = {INM-3},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406},
      pnm          = {5251 - Multilevel Brain Organization and Variability
                      (POF4-525) / DFG project 431549029 - SFB 1451:
                      Schlüsselmechanismen normaler und krankheitsbedingt
                      gestörter motorischer Kontrolle (431549029)},
      pid          = {G:(DE-HGF)POF4-5251 / G:(GEPRIS)431549029},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {38926677},
      UT           = {WOS:001255395200001},
      doi          = {10.1186/s12868-024-00876-x},
      url          = {https://juser.fz-juelich.de/record/1028966},
}