miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

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作者
Renkai Wang
Hao Zhang
Wenbin Ding
Zhenyu Fan
Boyao Ji
Chen Ding
Fang Ji
Hao Tang
机构
[1] Second Military Medical University,Department of Orthopedics, Changhai Hospital
[2] Hospital of Orthopedics,Guangdong Key Lab of Orthopedic Technology and Implant Materials, Key Laboratory of Trauma and Tissue Repair of Tropical Area of PLA
[3] General Hospital of Southern Theater Command of PLA,undefined
来源
Cell Death & Disease | / 11卷
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摘要
The regulation of bone formation and detailed mechanisms are still largely elusive, and the roles of microRNAs in this process have attracted much attention. Recently, a specific subtype of CD31hiendomucinhi (CD31hiEMCNhi) endothelium has been identified to promote bone formation, together with osteoblast development. However, the role of microRNA143 in the generation of CD31hi EMCNhi endothelium and bone formation remains unknown. In this study, we found that miR-143 was expressed both in osteoblast cells and CD31hiEMCNhi endothelial cells. Serum miR-143 level was negatively correlated with age in humans. Overexpression of miR-143 promoted osteoblast formation and angiogenic effects. Furthermore, CD31hiEmcnhi vessels and osteoblast formation were significantly inhibited in miR-143 knockout mice. Mechanistically, inhibitor HDAC7 was directly targeted by miR-143 and knockdown of HDAC7 was found to rescue the function of miR-143 deficiency. Thus, miR-143 promotes angiogenesis coupling with osteoblast differentiation by targeting HDAC7, which may serve as a potential target in angiogenic and osteogenic diseases.
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