AQP9: A novel target for bone loss induced by microgravity

被引:10
作者
Bu, Guoyun [1 ,2 ]
Shuang, Feng [1 ,3 ]
Wu, Ye [1 ]
Ren, Dongfeng [1 ]
Hou, Shuxun [1 ]
机构
[1] Chinese Peoples Liberat Army Gen Hosp, Affiliated Hosp 1, Dept Orthopaed, Inst Orthopaed, Beijing 100048, Peoples R China
[2] Nankai Univ, Sch Med, Tianjin 300071, Peoples R China
[3] 94th Hosp Chinese Peoples Liberat Army, Nanchang, Peoples R China
关键词
Aquaporin-9; Microgravity; Bone loss; Femur; Bone mineral density; OSTEOCLAST DIFFERENTIATION; KNOCKOUT MICE; BED REST; WEIGHTLESSNESS; SPACEFLIGHT; AQUAPORIN-9; TURNOVER; SPACE;
D O I
10.1016/j.bbrc.2012.02.100
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
The aim of current study was to elucidate whether aquaporin-9 (AQP9) expression was involved in the progression of bone loss induced by microgravity. We used the hind-limb suspension (HLS) mice model to simulate microgravity and induce bone loss. It was found that HLS exposure decreased femur bone mineral density (BMD), and enhanced femur AQP9 mRNA and protein levels. Then, the relationship between AQP9 mRNA expression and BMD was studied and it was showed that femur AQP9 mRNA level was negatively related to femur BMD in mice exposed to HLS. We sought to exam the function of AQP9 in the femur using the AQP9-null mice. It was found that AQP9 knockout attenuated bone loss and inhibited osteoclastogenesis under the condition of HLS exposure, but had no similar effect on bone under normal physiological conditions. In addition, it was found that exposure to simulated hypergravity or exercise training, main countermeasures against microgravity, reduced AQP9 mRNA and protein levels in femur of mice. Moreover, it was found that both aging and estrogen deprivation, another two risk factors of bone loss, had no significant effect on femur AQP9 expression. In conclusion, AQP9 plays an important role in the development of microgravity-induced bone loss, and may be a potential target for the prevention or management of microgravity-induced bone loss. (C) 2012 Elsevier Inc. All rights reserved.
引用
收藏
页码:774 / 778
页数:5
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