Control of bone formation by the serpentine receptor Frizzled-9.
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Control of bone formation by the serpentine receptor Frizzled-9. / Albers, Joachim; Schulze, Jochen; Beil, Frank Timo; Gebauer, Matthias; Baranowsky, Anke; Keller, Johannes; Marshall, Robert-Percy; Wintges, Kristofer; Friedrich, Felix; Priemel, Matthias; Schilling, Arndt; Rueger, Johannes Maria; Cornils, Kerstin; Fehse, Boris; Streichert, Thomas; Sauter, Guido; Jakob, Franz; Insogna, Karl L; Pober, Barbara; Knobeloch, Klaus-Peter; Francke, Uta; Amling, Michael; Schinke, Thorsten.
In: J CELL BIOL, Vol. 192, No. 6, 6, 2011, p. 1057-1072.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
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TY - JOUR
T1 - Control of bone formation by the serpentine receptor Frizzled-9.
AU - Albers, Joachim
AU - Schulze, Jochen
AU - Beil, Frank Timo
AU - Gebauer, Matthias
AU - Baranowsky, Anke
AU - Keller, Johannes
AU - Marshall, Robert-Percy
AU - Wintges, Kristofer
AU - Friedrich, Felix
AU - Priemel, Matthias
AU - Schilling, Arndt
AU - Rueger, Johannes Maria
AU - Cornils, Kerstin
AU - Fehse, Boris
AU - Streichert, Thomas
AU - Sauter, Guido
AU - Jakob, Franz
AU - Insogna, Karl L
AU - Pober, Barbara
AU - Knobeloch, Klaus-Peter
AU - Francke, Uta
AU - Amling, Michael
AU - Schinke, Thorsten
PY - 2011
Y1 - 2011
N2 - Although Wnt signaling in osteoblasts is of critical importance for the regulation of bone remodeling, it is not yet known which specific Wnt receptors of the Frizzled family are functionally relevant in this process. In this paper, we show that Fzd9 is induced upon osteoblast differentiation and that Fzd9(-/-) mice display low bone mass caused by impaired bone formation. Our analysis of Fzd9(-/-) primary osteoblasts demonstrated defects in matrix mineralization in spite of normal expression of established differentiation markers. In contrast, we observed a reduced expression of chemokines and interferon-regulated genes in Fzd9(-/-) osteoblasts. We also identified the ubiquitin-like modifier Isg15 as one potential downstream mediator of Fzd9 in these cells. Importantly, our molecular analysis further revealed that canonical Wnt signaling is not impaired in the absence of Fzd9, thus explaining the absence of a bone resorption phenotype. Collectively, our results reveal a previously unknown function of Fzd9 in osteoblasts, a finding that may have therapeutic implications for bone loss disorders.
AB - Although Wnt signaling in osteoblasts is of critical importance for the regulation of bone remodeling, it is not yet known which specific Wnt receptors of the Frizzled family are functionally relevant in this process. In this paper, we show that Fzd9 is induced upon osteoblast differentiation and that Fzd9(-/-) mice display low bone mass caused by impaired bone formation. Our analysis of Fzd9(-/-) primary osteoblasts demonstrated defects in matrix mineralization in spite of normal expression of established differentiation markers. In contrast, we observed a reduced expression of chemokines and interferon-regulated genes in Fzd9(-/-) osteoblasts. We also identified the ubiquitin-like modifier Isg15 as one potential downstream mediator of Fzd9 in these cells. Importantly, our molecular analysis further revealed that canonical Wnt signaling is not impaired in the absence of Fzd9, thus explaining the absence of a bone resorption phenotype. Collectively, our results reveal a previously unknown function of Fzd9 in osteoblasts, a finding that may have therapeutic implications for bone loss disorders.
M3 - SCORING: Journal article
VL - 192
SP - 1057
EP - 1072
JO - J CELL BIOL
JF - J CELL BIOL
SN - 0021-9525
IS - 6
M1 - 6
ER -
