GDF11 decreases bone mass by stimulating osteoclastogenesis and inhibiting osteoblast differentiation

Weiqing Liu, Liyan Zhou, Chenchen Zhou, Shiwen Zhang, Junjun Jing, Liang Xie, Ningyuan Sun, Xiaobo Duan, Wei Jing, Xing Liang, Hu Zhao, Ling Ye, Qianming Chen and Quan Yuan ()
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Weiqing Liu: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Liyan Zhou: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Chenchen Zhou: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Shiwen Zhang: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Junjun Jing: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Liang Xie: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Ningyuan Sun: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Xiaobo Duan: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Wei Jing: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Xing Liang: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Hu Zhao: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Ling Ye: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Qianming Chen: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University
Quan Yuan: State Key Laboratory of Oral diseases, West China Hospital of Stomatology, Sichuan University

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract 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 through Smad2/3 and c-Fos-dependent induction of Nfatc1. Injection of GDF11 impairs bone regeneration in mice and blocking GDF11 function prevents oestrogen-deficiency-induced bone loss and ameliorates age-related osteoporosis. Our data demonstrate that GDF11 is a previously unrecognized regulator of bone remodelling and suggest that GDF11 is a potential target for treatment of osteoporosis.

Date: 2016
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DOI: 10.1038/ncomms12794

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