% 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{Baldauf:284042,
      author       = {Baldauf, Conny K and Poschmann, Linda and Edelmann-Stephan,
                      Bärbel and Angenstein, Frank and Haage, Tobias R and
                      Bhuria, Vikas and Philipsen, Lars and Berlin, Hannes and
                      Dieterich, Daniela C and Böttcher, Martin and Mougiakakos,
                      Dimitrios and Schraven, Burkhart and Fischer, Thomas},
      title        = {{I}ntegrin-dependence of extramedullary erythropoiesis in
                      the spleen of {J}ak2-{V}617{F} positive myeloproliferative
                      neoplasm in mice.},
      journal      = {Experimental hematology},
      volume       = {154},
      issn         = {0531-5573},
      address      = {Amsterdam [u.a.]},
      publisher    = {Elsevier Science},
      reportid     = {DZNE-2026-00077},
      pages        = {105340},
      year         = {2026},
      abstract     = {The molecular mechanisms driving splenomegaly in
                      myeloproliferative neoplasms (MPNs) remain poorly
                      understood. Utilizing the Jak2-V617F knock-in mouse model,
                      we investigated the role of β1- and β2-integrins in
                      regulating spleen volume and spleen weight. The response to
                      neutralizing antibodies against VLA-4 and the β2-integrin
                      chain, as well as to isotype controls, was evaluated by
                      serial intraindividual magnetic resonance imaging, by
                      assessment of spleen weight and by analysis of the cellular
                      composition of spleens. Short-term anti-VLA-4/β2-integrin
                      treatment (applied on day 1 and evaluated at day 8)
                      significantly reduced the spleen volume by $30\%$ compared
                      with the immunoglobulin G (IgG) control. At the cellular
                      level, anti-integrin treatment led to a substantial $30\%$
                      decrease in erythroblast counts and a $23\%$ reduction in
                      basophilic erythroblasts within the spleen, as compared with
                      the isotype control. Furthermore, immunohistochemistry
                      analysis of spleen sections revealed that CD71 (=
                      Transferrin receptor protein 1) expression in spleen
                      remained largely unchanged, whereas there was a clear
                      reduction in Ter119 expression upon anti-integrin treatment.
                      These data suggest that the substantial decrease in
                      erythroblasts following anti-integrin treatment is a primary
                      factor contributing to the overall reduction in spleen size.
                      To study the spleen architecture, multiepitope ligand
                      cartography (MELC) analysis of spleen sections was applied.
                      This demonstrated that the spatial distribution of the
                      marginal zone, red pulp, and white pulp remained unaltered
                      upon anti-integrin treatment in JAK2-V617F knock-in mice. In
                      summary, the present study identified a previously
                      unrecognized role of the β1-integrin VLA-4 and of
                      β2-integrin chains in extramedullary erythropoiesis of the
                      spleen in JAK2-V617F-induced disease.},
      keywords     = {Animals / Janus Kinase 2: genetics / Janus Kinase 2:
                      metabolism / Spleen: pathology / Spleen: metabolism / Mice /
                      Myeloproliferative Disorders: genetics / Myeloproliferative
                      Disorders: pathology / Myeloproliferative Disorders:
                      metabolism / Erythropoiesis: genetics / Integrin
                      alpha4beta1: genetics / Integrin alpha4beta1: metabolism /
                      Integrin alpha4beta1: immunology / CD18 Antigens: genetics /
                      CD18 Antigens: metabolism / CD18 Antigens: immunology /
                      Hematopoiesis, Extramedullary / Integrin beta1: metabolism /
                      Integrin beta1: genetics / Splenomegaly: genetics /
                      Splenomegaly: pathology / Erythroblasts: pathology /
                      Erythroblasts: metabolism / Janus Kinase 2 (NLM Chemicals) /
                      Jak2 protein, mouse (NLM Chemicals) / Integrin alpha4beta1
                      (NLM Chemicals) / CD18 Antigens (NLM Chemicals) / Integrin
                      beta1 (NLM Chemicals)},
      cin          = {AG Angenstein},
      ddc          = {610},
      cid          = {I:(DE-2719)1310004},
      pnm          = {351 - Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:41360369},
      doi          = {10.1016/j.exphem.2025.105340},
      url          = {https://pub.dzne.de/record/284042},
}