The coupling of reduced type H vessels with unloading-induced bone loss and the protection role of Panax quinquefolium saponin in the male mice

被引:43
作者
Liang, Shuai [1 ,2 ,3 ]
Ling, Shukuan [2 ]
Du, Ruikai [2 ]
Li, Yuheng [2 ]
Liu, Caizhi [2 ]
Shi, Junhe [4 ]
Gao, Jie [1 ]
Sun, Weijia [2 ]
Li, Jianwei [2 ]
Zhong, Guohui [2 ]
Liu, Zizhong [2 ]
Zhao, Dingsheng [2 ]
Sun, Huiyuan [5 ]
Li, Yang [6 ]
Yuan, Xinxin [2 ]
Qu, Hua [1 ]
Jin, Xiaoyan [2 ]
Li, Dong [6 ]
Shi, Dazhuo [1 ]
Li, Yingxian [2 ]
机构
[1] China Acad Chinese Med Sci, Xiyuan Hosp, 1 Xiyuan Cao Chang Rd, Beijing, Peoples R China
[2] China Astronaut Res & Training Ctr, State Key Lab Space Med Fundamentals & Applicat, Beiqing Rd, Beijing, Peoples R China
[3] Beijing Univ Chinese Med, Dongfang Hosp, Beijing, Peoples R China
[4] Univ Illinois, Coll Dent, Ctr Wound Healing & Tissue Regenerat, 801 S Paulina St, Chicago, IL 60612 USA
[5] Beijing Univ, Chinese Med Affiliated Hosp 3, Beijing, Peoples R China
[6] Beijing Inst Life, Beijing Proteome Res Ctr, Natl Ctr Prot Sci Beijing, State Key Lab Prote, Beijing, Peoples R China
基金
中国国家自然科学基金; 中国博士后科学基金;
关键词
Bone loss; Unloading; Type H vessel; PQS; Osteogenesis; ATTENUATES CARDIOMYOCYTE APOPTOSIS; ANGIOGENESIS; OSTEOGENESIS; OSTEOBLAST;
D O I
10.1016/j.bone.2020.115712
中图分类号
R5 [内科学];
学科分类号
100201 [内科学];
摘要
Unloading-induced bone loss is a critical complication characterized by the imbalance of bone formation and resorption induced by long-term confinement in bed or spaceflight. CD31(hi)Emcn(hi) (type H) vessel is a specific subtype of capillary, which was coupled with osteogenesis. However, the change of type H vessel and its contributions to the unloading-induced bone loss remains undisclosed. Herein, we found that bone formation and the number of type H vessels were synchronously reduced in the hindlimb-unloading (HU) mice. Panax quinquefolium saponin (PQS) could increase bone mass, osteoblast function and the number of type H vessels in the HU mice. In vitro, PQS treatment accelerated HMECs migration, augmented the total tube loops and increased the secretion of VEGF and Noggin. Primary osteoblasts function was obviously increased when treated with supernatant from PQS-treated HMECs. These effects of PQS were substantially counteracted when VEGF and Noggin in HMECs were knocked down by siRNA. These results demonstrated that unloading-induced bone loss is coupled with reduction of type H vessels and PQS performs preventive function via promoting type H vessel angiogenesis, which is closely associated with endothelial cell-derived VEGF and Noggin.
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页数:12
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