The group of Michael Schupp, together with cooperation partners from the German Institute for Nutrition Research in Potsdam, the Julius Wolff Institute of Biomechanics and Musculoskeletal Regeneration of the Charité, and the Max Planck Institute for Molecular Genetics Berlin, gained new insights into the function of the transcription factor GATA2 in bone homeostasis. GATA2 binds to regulatory DNA elements and controls the expression of genes that determine the differentiation of bone anabolic osteoblasts. Specific deletion of GATA2 in osteogenic progenitor cells in mice resulted in reduced density and mechanical stability of bones and changes in the blood counts. Since GATA2 has been mainly associated with blood cell differentiation / hematopoiesis, GATA2 seems to exert an additional influence by its function in bone homeostasis since hematopoiesis takes place in precisely those bone regions. These findings could provide the basis for new therapeutic approaches to diseases of the skeletal system and highlight the interactions between bone structure and hematopoiesis.
Original work:
Tolkachov A, Fischer C, Ambrosi TH, Bothe M, Han CT, Muenzner M, Mathia S, Salminen M, Seifert G, Thiele M, Duda GN, Meijsing SH, Sauer S, Schulz TJ, Schupp M.
Loss of the hematopoietic stem cell factor GATA2 in the osteogenic lineage impairs trabecularization and mechanical strength of bone.
Mol Cell Biol. 2018 Mar 26. pii: MCB.00599-17. doi: 10.1128/MCB.00599-17. [Epub ahead of print], PMID: 29581184
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