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@ARTICLE{Heinisch:905217,
      author       = {Heinisch, Ole and Zeyen, Thomas and Goldmann, Tobias and
                      Prinz, Marco and Huber, Michael and Jung, Jennifer and Arik,
                      Eren and Habib, Shahin and Slowik, Alexander and Reich, Arno
                      and Schulz, Jörg B. and Habib, Pardes},
      title        = {{E}rythropoietin {A}brogates {P}ost-{I}schemic {A}ctivation
                      of the {NLRP}3, {NLRC}4, and {AIM}2 {I}nflammasomes in
                      {M}icroglia/{M}acrophages in a {TAK}1-{D}ependent {M}anner},
      journal      = {Translational stroke research},
      volume       = {13},
      issn         = {1868-4483},
      address      = {New York, NY},
      publisher    = {Springer},
      reportid     = {FZJ-2022-00500},
      pages        = {462–482},
      year         = {2022},
      abstract     = {Inflammasomes are known to contribute to brain damage after
                      acute ischemic stroke (AIS). TAK1 is predominantly expressed
                      in microglial cells and can regulate the NLRP3 inflammasome,
                      but its impact on other inflammasomes including NLRC4 and
                      AIM2 after AIS remains elusive. EPO has been shown to reduce
                      NLRP3 protein levels in different disease models. Whether
                      EPO-mediated neuroprotection after AIS is conveyed via an
                      EPO/TAK1/inflammasome axis in microglia remains to be
                      clarified. Subjecting mice deficient for TAK1 in
                      microglia/macrophages (Mi/MΦ) to AIS revealed a significant
                      reduction in infarct sizes and neurological impairments
                      compared to the corresponding controls. Post-ischemic
                      increased activation of TAK1, NLRP3, NLRC4, and AIM2
                      inflammasomes including their associated downstream cascades
                      were markedly reduced upon deletion of Mi/MΦ TAK1. EPO
                      administration improved clinical outcomes and dampened
                      stroke-induced activation of TAK1 and inflammasome cascades,
                      which was not evident after the deletion of Mi/MΦ TAK1.
                      Pharmacological inhibition of NLRP3 in microglial BV-2 cells
                      did not influence post-OGD IL-1β levels, but increased
                      NLRC4 and AIM2 protein levels, suggesting compensatory
                      activities among inflammasomes. Overall, we provide evidence
                      that Mi/MΦ TAK1 regulates the expression and activation of
                      the NLRP3, NLRC4, AIM2 inflammasomes. Furthermore, EPO
                      mitigated stroke-induced activation of TAK1 and
                      inflammasomes, indicating that EPO conveyed neuroprotection
                      might be mediated via an EPO/TAK1/inflammasome axis.},
      cin          = {INM-11},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-11-20170113},
      pnm          = {5252 - Brain Dysfunction and Plasticity (POF4-525)},
      pid          = {G:(DE-HGF)POF4-5252},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {34628598},
      UT           = {WOS:000705686300001},
      doi          = {10.1007/s12975-021-00948-8},
      url          = {https://juser.fz-juelich.de/record/905217},
}