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@ARTICLE{Butt:285264,
      author       = {Butt, Umer Javed and Çakır, Umut and Wildenburg,
                      Anne-Fleur and Curto, Yasmina and Ye, Liu and Bansal, Vikas
                      and Boretius, Susann and Nave, Klaus-Armin and Singh,
                      Manvendra and Ehrenreich, Hannelore},
      title        = {{F}orebrain-specific loss of erythropoietin provokes
                      compensatory upregulation of different {EPO} receptors.},
      journal      = {Molecular psychiatry},
      volume       = {31},
      number       = {3},
      issn         = {1359-4184},
      address      = {[London]},
      publisher    = {Springer Nature},
      reportid     = {DZNE-2026-00206},
      pages        = {1241 - 1252},
      year         = {2026},
      abstract     = {The procognitive growth factor erythropoietin (EPO) and its
                      canonical receptor, EPOR, have long been recognized to be
                      expressed by most cell types in the brain. Cognitive
                      domains, improved by injections of exogenous EPO or by
                      endogenous, hypoxia-stimulated EPO, include important
                      forebrain functions, namely attention, working memory,
                      drive, and executive performance. To gain mechanistic
                      insight into the involvement of forebrain-expressed EPO, we
                      deleted EPO in mice using as specific cre-driver Emx1. Here,
                      we report that these mutant mice act comparably to their
                      wildtype littermates in a comprehensive behavioral test
                      battery. Importantly, we find that the transcripts of both
                      EPOR and a novel, brain-expressed EPO receptor, EphB4,
                      respond to EPO deletion with compensatory upregulation.
                      EphB4 expression in brain and its increase upon forebrain
                      erasure of EPOR are confirmed by in situ hybridization and
                      immunohistochemistry. The augmented expression of both EPOR
                      and EphB4 and their regulatory intercorrelation may explain
                      why EmxEPO mutants show an even superior performance in the
                      most challenging working memory task. Using the previously
                      published single-nuclei-RNA-seq dataset, we further confirm
                      the suggested compensatory mechanism, wherein EPO loss or
                      reduction drives elevated EPOR expression, adding another
                      layer to the intricate regulation of EPO signaling in
                      hippocampal pyramidal neurons. Collectively, these data may
                      explain the lack of behavioral and negative cognitive
                      consequences upon forebrain-wide EPO elimination.},
      keywords     = {Animals / Erythropoietin: metabolism / Erythropoietin:
                      genetics / Prosencephalon: metabolism / Receptors,
                      Erythropoietin: metabolism / Receptors, Erythropoietin:
                      genetics / Mice / Memory, Short-Term: physiology /
                      Up-Regulation / Receptor, EphB4: metabolism / Receptor,
                      EphB4: genetics / Male / Hippocampus: metabolism / Signal
                      Transduction / Brain: metabolism / Mice, Inbred C57BL /
                      Mice, Transgenic / Mice, Knockout / Cognition: physiology /
                      Erythropoietin (NLM Chemicals) / Receptors, Erythropoietin
                      (NLM Chemicals) / Receptor, EphB4 (NLM Chemicals) / Epo
                      protein, mouse (NLM Chemicals)},
      cin          = {AG Bansal},
      ddc          = {610},
      cid          = {I:(DE-2719)1210013},
      pnm          = {354 - Disease Prevention and Healthy Aging (POF4-354)},
      pid          = {G:(DE-HGF)POF4-354},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41028570},
      doi          = {10.1038/s41380-025-03230-7},
      url          = {https://pub.dzne.de/record/285264},
}