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J. Biol. Chem., Vol. 278, Issue 19, 17360-17367, May 9, 2003

This Article Full Text Full Text (PDF) All Versions of this Article: 278/19/17360    most recent M207631200v1 Submit a Letter to Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Stock, M. Articles by Otto, F. Search for Related Content PubMed PubMed Citation Articles by Stock, M. Articles by Otto, F. Social Bookmarking                      What's this?

Expression of Galectin-3 in Skeletal Tissues Is Controlled by Runx2^*

Michael Stock^§, Henning Schäfer, Sigmar Stricker^¶, Gerhard Gross, Stefan Mundlos^¶, and Florian Otto^**

From the  Division of Hematology/Oncology, Medical Center and the ^§ Institute for Biology I, University of Freiburg, 79106 Freiburg, Germany, the ^¶ Max Planck Institute for Molecular Genetics, 14195 Berlin, Germany, and the  Gesellschaft für Biotechnologische Forschung, 38124 Braunschweig, Germany

The -galatoside-specific lectin galectin-3 is expressed in vivo in osteoblasts as well as in epiphyseal cartilage. Here we show that in vitro, galectin-3 expression is up-regulated in the preosteoblastic cell line MC3T3-E1 during the matrix maturation stage of the osteoblast developmental sequence. Expression persists into late differentiation stages when the mature osteoblastic phenotype is established. The skeletal expression pattern of galectin-3 overlaps at many sites with that of the transcription factor Runx2. Runx2 is a key regulator of osteoblast development and necessary for chondrocyte differentiation in the growth plate. Both human and mouse galectin-3 promoters contain putative Runx-binding sites. The constitutive or inducible forced expression of Runx2 is sufficient for the onset of galectin-3 transcription in the mesenchymal precursor cell line C3H10T1/2. Moreover, Runx2 is able to bind to at least two sites in the galectin-3 promoter region. The crucial role of Runx2 was confirmed in Runx2-deficient mice, which are devoid of galectin-3 expression in skeletal cells. The overlapping expression pattern of galectin-3 with the other two members of the Runt family of transcription factors (Runx1 and Runx3) points to a potential regulation of the galectin-3 gene (LGALS3) by these factors in hematopoietic, skin, and dorsal root ganglial cells.

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