miR-143 promotes angiogenesis and osteoblast differentiation by targeting HDAC7

被引:48
|
作者
Wang, Renkai [1 ,2 ]
Zhang, Hao [1 ]
Ding, Wenbin [1 ]
Fan, Zhenyu [1 ]
Ji, Boyao [1 ]
Ding, Chen [1 ]
Ji, Fang [1 ]
Tang, Hao [1 ]
机构
[1] Second Mil Med Univ, Changhai Hosp, Dept Orthoped, Shanghai, Peoples R China
[2] Gen Hosp Southern Theater Command PLA, Hosp Orthoped, Guangdong Key Lab Orthoped Technol & Implant Mat, Key Lab Trauma & Tissue Repair Trop Area PLA, 111 Liuhua Rd, Guangzhou 510010, Guangdong, Peoples R China
基金
中国国家自然科学基金;
关键词
HISTONE DEACETYLASES; BONE; APOPTOSIS; BETA; OSTEOSARCOMA; PROLIFERATION; OSTEOGENESIS; INHIBITION; BIOGENESIS; OSTERIX;
D O I
10.1038/s41419-020-2377-4
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
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 CD31(hi)endomucin(hi) (CD31(hi)EMCN(hi)) endothelium has been identified to promote bone formation, together with osteoblast development. However, the role of microRNA143 in the generation of CD31(hi) EMCNhi endothelium and bone formation remains unknown. In this study, we found that miR-143 was expressed both in osteoblast cells and CD31(hi)EMCN(hi) endothelial cells. Serum miR-143 level was negatively correlated with age in humans. Overexpression of miR-143 promoted osteoblast formation and angiogenic effects. Furthermore, CD31(hi)Emcn(hi) 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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页数:15
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