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Erben, R.G.* ; Zeitz, U.* ; Weber, K.* ; Stierstorfer, B.* ; Wolf, G.* ; Schmahl, W.* ; Balling, R. ; Quintanilla-Martinez, L.

A non-functioning vitamin D receptor predisposes to leukaemoid reactions in mice.

Hematol. Oncol. 28, 185-191 (2010)
DOI PMC
Open Access Green möglich sobald Postprint bei der ZB eingereicht worden ist.
The vitamin D hormone 1,25-dihydroxyvitamin D(3) [1,25(OH)(2) D(3) ], the biologically active form of vitamin D, is not only essential for mineral metabolism but may have important functions beyond calcium homoeostasis. By gene targeting, we have recently generated mice expressing a functionally inactive mutant vitamin D receptor (VDR). After a change in environmental conditions from specific pathogen free (SPF) conditions to a modified barrier system, a high percentage of aged mutant, but not wild-type, mice developed a haematological disorder characterized by splenomegaly, granulocytosis, thrombocytosis and dysplastic changes with displacement of erythropoiesis in bone marrow during the following months. All cases were associated with very high serum levels of the acute phase reaction protein serum amyloid A (SAA). Serological testing of affected mice revealed antibodies against murine hepatitis virus (MHV). However, electron microscopy of spleen and bone marrow cells did not reveal virus particles, and clinical signs of infectious diseases were absent. We hypothesize that a non-functioning VDR is associated with a latent defect in the regulation of myeloid cell differentiation and proliferation. Under the conditions of environmental stress, this latent defect may predispose to a deregulation of myelopoiesis in the form of a leukaemoid reaction accompanied by dysplastic changes. Thus, 1,25(OH)(2) D(3) may be an important inhibitory factor in the onset and progression of myeloproliferative and myelodysplastic diseases.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter vitamin D; leukaemoid reaction; chronic myeloid leukaemia; mice
Sprache
Veröffentlichungsjahr 2010
HGF-Berichtsjahr 2010
ISSN (print) / ISBN 0278-0232
e-ISSN 1099-1069
Zeitschrift Hematological Oncology
Quellenangaben Band: 28, Heft: 4, Seiten: 185-191 Artikelnummer: , Supplement: ,
Verlag Wiley
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Developmental Genetics (IDG)
Institute of Pathology (PATH)
POF Topic(s) 30204 - Cell Programming and Repair
30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Genetics and Epidemiology
Enabling and Novel Technologies
PSP-Element(e) G-500500-001
G-500300-001
PubMed ID 20301229
DOI 10.1002/hon.938
Scopus ID 78650046371
Erfassungsdatum 2010-12-31
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