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  • 1
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    German Medical Science GMS Publishing House; Düsseldorf
    In:  Deutscher Kongress für Orthopädie und Unfallchirurgie; 75. Jahrestagung der Deutschen Gesellschaft für Unfallchirurgie, 97. Tagung der Deutschen Gesellschaft für Orthopädie und Orthopädische Chirurgie, 52. Tagung des Berufsverbandes der Fachärzte für Orthopädie; 20111025-20111028; Berlin; DOCGR13-1456 /20111018/
    Publication Date: 2011-10-18
    Keywords: ddc: 610
    Language: English
    Type: conferenceObject
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  • 2
    Keywords: CELLS ; proliferation ; DIFFERENTIATION ; HEALTH ; BONE-FORMATION ; OSTEOPOROSIS ; POSTMENOPAUSAL WOMEN ; RANDOMIZED CONTROLLED-TRIAL ; RECEPTOR-ALPHA ; CANCELLOUS BONE
    Abstract: Postmenopausal osteoporosis is characterized by declining estrogen levels, and estrogen replacement therapy has been proven beneficial for preventing bone loss in affected women. While the physiological functions of estrogen in bone, primarily the inhibition of bone resorption, have been studied extensively, the effects of pharmacological estrogen administration are still poorly characterized. Since elevated levels of follicle-stimulating hormone (FSH) have been suggested to be involved in postmenopausal bone loss, we investigated whether the skeletal response to pharmacological estrogen administration is mediated in a FSH-dependent manner. Therefore, we treated wildtype and FSHbeta-deficicent (Fshb(-/-)) mice with estrogen for 4 weeks and subsequently analyzed their skeletal phenotype. Here we observed that estrogen treatment resulted in a significant increase of trabecular and cortical bone mass in both, wildtype and Fshb(-/-) mice. Unexpectedly, this FSH-independent pharmacological effect of estrogen was not caused by influencing bone resorption, but primarily by increasing bone formation. To understand the cellular and molecular nature of this osteo-anabolic effect we next administered estrogen to mouse models carrying cell specific mutant alleles of the estrogen receptor alpha (ERalpha). Here we found that the response to pharmacological estrogen administration was not affected by ERalpha inactivation in osteoclasts, while it was blunted in mice lacking the ERalpha in osteoblasts or in mice carrying a mutant ERalpha incapable of DNA binding. Taken together, our findings reveal a previously unknown osteo-anabolic effect of pharmacological estrogen administration, which is independent of FSH and requires DNA-binding of ERalpha in osteoblasts.
    Type of Publication: Journal article published
    PubMed ID: 23209701
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  • 3
    Keywords: EXPRESSION ; MICE ; MOUSE ; MULTIPLE-MYELOMA ; MASS ; OSTEOBLAST DIFFERENTIATION ; RECEPTOR-RELATED PROTEIN-5 ; SOST GENE ; SCLEROSTIN ; LRP5 GENE
    Abstract: Wnt signalling is a key pathway controlling bone formation in mice and humans. One of the regulators of this pathway is Dkk1, which antagonizes Wnt signalling through the formation of a ternary complex with the transmembrane receptors Krm1/2 and Lrp5/6, thereby blocking the induction of Wnt signalling by the latter ones. Here we show that Kremen-2 (Krm2) is predominantly expressed in bone, and that its osteoblast-specific over-expression in transgenic mice (Col1a1-Krm2) results in severe osteoporosis. Histomorphometric analysis revealed that osteoblast maturation and bone formation are disturbed in Col1a1-Krm2 mice, whereas bone resorption is increased. In line with these findings, primary osteoblasts derived from Col1a1-Krm2 mice display a cell-autonomous differentiation defect, impaired canonical Wnt signalling and decreased production of the osteoclast inhibitory factor Opg. To determine whether the observed effects of Krm2 on bone remodeling are physiologically relevant, we analyzed the skeletal phenotype of 24 weeks old Krm2-deficient mice and observed high bone mass caused by a more than three-fold increase in bone formation. Taken together, these data identify Krm2 as a regulator of bone remodeling and raise the possibility that antagonizing KRM2 might prove beneficial in patients with bone loss disorders.
    Type of Publication: Journal article published
    PubMed ID: 20436912
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