Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

Effect of GDF11 on RANKL-induced osteoclastogenesis

ABSTRACT: GDF11 treatment leads to bone loss in mice and strongly stimulates RANKL-induced osteoclastogenesis of bone marrow-derived macrophages (BMMs) in vitro. We used microarrays to identified distinct classes of up-regulated genes in BMMs after GDF11 treatment. Mouse BMMs were treated with or without GDF11 for RNA extraction and and hybridization on Affymetrix microarrays

ORGANISM(S): Mus musculus

SUBMITTER: Quan Yuan

PROVIDER: E-GEOD-84609 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation.

Liu Weiqing W Zhou Liyan L Zhou Chenchen C Zhang Shiwen S Jing Junjun J Xie Liang L Sun Ningyuan N Duan Xiaobo X Jing Wei W Liang Xing X Zhao Hu H Ye Ling L Chen Qianming Q Yuan Quan Q

Nature communications 20160922

Osteoporosis is an age-related disease that affects millions of people. Growth differentiation factor 11 (GDF11) is a secreted member of the transforming growth factor beta (TGF-β) superfamily. Deletion of Gdf11 has been shown to result in a skeletal anterior-posterior patterning disorder. Here we show a role for GDF11 in bone remodelling. GDF11 treatment leads to bone loss in both young and aged mice. GDF11 inhibits osteoblast differentiation and also stimulates RANKL-induced osteoclastogenesis ...[more]

PMID: 27653144

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Project description:Bone remodeling is characterized by the sequential, local tethering of osteoclasts and osteoblasts, and is key to the maintenance of bone integrity. While bone matrix-mobilized growth factors, such as TGF-β, are proposed to regulate remodeling, no in vivo evidence exists that an osteoclast-produced molecule is the enigmatic coupling factor. We have identified Cthrc1, a protein secreted by mature bone-resorbing osteoclasts, that targets stromal cells so as to stimulate osteogenesis. The expression of Cthrc1 is robustly induced when mature osteoclasts are placed on dentin or hydroxyapatite, and also by increasing extracellular calcium. Cthrc1 expression in bone increases in a high turnover state, such as that which is induced by RANKL injections in vivo, whereas it decreases with aging or following alendronate treatment, conditions associated with suppressed bone turnover. The targeted deletion of the Cthrc1 gene eliminates Cthrc1 expression in bone, whereas its deficiency in osteoblasts does not exert any significant effect. Osteoclast-specific deletion of the Cthrc1 gene results in osteopenia due to reduced bone formation: it also impairs the coupling process following resorption induced by RANKL injections, with a resultant impairment of bone mass recovery. Thus, Cthrc1 is an osteoclast-secreted “coupling factor” that regulates bone remodeling and hence, skeletal integrity. Total bone marrow cells were prepared from the femurs and tibias of 8-10-week-old C57BL/6 mice and cultured in the presence of M-CSF (100ng/ml) for 3 days as described previously (Takeshita et al., 2000 JBMR 15:1477-1488). Cells were harvested with 0.02% EDTA/PBS and used as bone marrow macrophages (BMMs). These BMMs were cultured in the presence of M-CSF (100 ng/ml) and RANKL (100ng/ml) for 2 days. TRAP positive mononuclear cells were harvested and used as pre-osteoclasts (pOC). These pOC cells were further cultured in the presence of M-CSF and RANKL for 2 days in normal plastic plate or on dentin slices. After 2 days, multinucleated TRAP positive mature osteoclasts were generated as mature osteoclasts on plate (mOCp) and mature resorbing osteoclasts on dentin (mOCd), respectively. RNAs were extracted from four different stages of osteoclast lineage cells; BMMs, pOC, mOCp and mOCd, and used for microarray analysis.

Dataset Information

Effect of GDF11 on RANKL-induced osteoclastogenesis

Publications

GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation.

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