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333 results on '"Wang, Aiyuan"'

11. 3D-printed cell-free PCL–MECM scaffold with biomimetic micro-structure and micro-environment to enhance in situ meniscus regeneration

Author

Guo, Weimin, Chen, Mingxue, Wang, Zhenyong, Tian, Yue, Zheng, Jinxuan, Gao, Shuang, Li, Yangyang, Zheng, Yufeng, Li, Xu, Huang, Jingxiang, Niu, Wei, Jiang, Shuangpeng, Hao, Chunxiang, Yuan, Zhiguo, Zhang, Yu, Wang, Mingjie, Wang, Zehao, Peng, Jiang, Wang, Aiyuan, Wang, Yu, Sui, Xiang, Xu, Wenjing, Hao, Libo, Zheng, Xifu, Liu, Shuyun, and Guo, Quanyi

Published
2021
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35. Mechanical stimulation controls osteoclast function through the regulation of Ca2+-activated Cl− channel Anoctamin 1.

Author

Sun, Weijia, Li, Yuheng, Li, Jianwei, Tan, Yingjun, Yuan, Xinxin, Meng, Haoye, Ye, Jianting, Zhong, Guohui, Jin, XiaoYan, Liu, Zizhong, Du, Ruikai, Xing, Wenjuan, Zhao, Dingsheng, Song, Jinping, Li, Youyou, Pan, Junjie, Zhao, Yunzhang, Li, Qi, Wang, Aiyuan, and Ling, Shukuan

Subjects
BONE resorption, OSTEOCLAST inhibition, BONE cells, BONE remodeling, STRAINS & stresses (Mechanics), OSTEOCLASTS, CALCIUM ions
Abstract

Mechanical force loading is essential for maintaining bone homeostasis, and unloading exposure can lead to bone loss. Osteoclasts are the only bone resorbing cells and play a crucial role in bone remodeling. The molecular mechanisms underlying mechanical stimulation-induced changes in osteoclast function remain to be fully elucidated. Our previous research found Ca2+-activated Cl− channel Anoctamin 1 (Ano1) was an essential regulator for osteoclast function. Here, we report that Ano1 mediates osteoclast responses to mechanical stimulation. In vitro, osteoclast activities are obviously affected by mechanical stress, which is accompanied by the changes of Ano1 levels, intracellular Cl− concentration and Ca2+ downstream signaling. Ano1 knockout or calcium binding mutants blunts the response of osteoclast to mechanical stimulation. In vivo, Ano1 knockout in osteoclast blunts loading induced osteoclast inhibition and unloading induced bone loss and. These results demonstrate that Ano1 plays an important role in mechanical stimulation induced osteoclast activity changes. An essential role of the Ca2+-activated Cl− channel, Anoctamin 1, is identified in mediating the response of osteoclasts to mechanical stimulation. Ano1 knockout in osteoclasts inhibits unloading- induced osteoclast activation and unloading-induced bone loss. [ABSTRACT FROM AUTHOR]

Published
2023
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42. Xenoimplantation of an Extracellular-Matrix-Derived, Biphasic, Cell-Scaffold Construct for Repairing a Large Femoral-Head High-Load-Bearing Osteochondral Defect in a Canine Model

Author

Yang Qiang, Zhao Yanhong, Peng Jiang, Lu Shibi, Guo Quanyi, Ma Xinlong, Xia Qun, Xu Baoshan, Zhao Bin, Wang Aiyuan, Zhang Li, Xu Wengjing, and Zeng Chao

Subjects
Technology, Medicine, Science
Abstract

This study was aimed to develop an ECM-derived biphasic scaffold and to investigate its regeneration potential loaded with BM-MSCs in repair of large, high-load-bearing osteochondral defects of the canine femoral head. The scaffolds were fabricated using cartilage and bone ECM as a cartilage and bone layer, respectively. Osteochondral constructs were fabricated using induced BM-MSCs and the scaffold. Osteochondral defects (11 mm diameter × 10 mm depth) were created on femoral heads of canine and treated with the constructs. The repaired tissue was evaluated for gross morphology, radiography, histological, biomechanics at 3 and 6 months after implantation. Radiography revealed that femoral heads slightly collapsed at 3 months and severely collapsed at 6 months. Histology revealed that some defects in femoral heads were repaired, but with fibrous tissue or fibrocartilage, and femoral heads with different degrees of collapse. The bone volume fraction was lower for subchondral bone than normal femoral bone at 3 and 6 months. Rigidity was lower in repaired subchondral bone than normal femoral bone at 6 months. The ECM-derived, biphasic scaffold combined with induced BM-MSCs did not successfully repair large, high-load-bearing osteochondral defects of the canine femoral head. However, the experience can help improve the technique of scaffold fabrication and vascularization.

Published
2014
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43. MiR-214 targets ATF4 to inhibit bone formation

Author

Wang, Xiaogang, Guo, Baosheng, Li, Qi, Peng, Jiang, Yang, Zhijun, Wang, Aiyuan, Li, Dong, Hou, Zhibo, Lv, Ke, Kan, Guanghan, Cao, Hongqing, Wu, Heng, Song, Jinping, Pan, Xiaohua, Sun, Qiao, Ling, Shukuan, Li, Yuheng, Zhu, Mu, Zhang, Pengfei, Peng, Songlin, Xie, Xiaoqing, Tang, Tao, Hong, An, Bian, Zhaoxiang, Bai, Yanqiang, Lu, Aiping, Li, Yinghui, He, Fuchu, Zhang, Ge, and Li, Yingxian

Subjects
Bone regeneration -- Physiological aspects -- Health aspects -- Genetic aspects, MicroRNA -- Physiological aspects -- Health aspects, Biological sciences, Health
Abstract

Emerging evidence indicates that microRNAs (miRNAs) have important roles in regulating osteogenic differentiation and bone formation. Thus far, no study has established the pathophysiological role for miRNAs identified in human osteoporotic bone specimens. Here we found that elevated miR-214 levels correlated with a lower degree of bone formation in bone specimens from aged patients with fractures. We also found that osteoblast-specific manipulation of miR-214 levels by miR-214 antagomir treatment in miR-214 transgenic, ovariectomized, or hindlimb-unloaded mice revealed an inhibitory role of miR-214 in regulating bone formation. Further, in vitro osteoblast activity and matrix mineralization were promoted by antagomir-214 and decreased by agomir-214, and miR-214 directly targeted ATF4 to inhibit osteoblast activity. These data suggest that miR-214 has a crucial role in suppressing bone formation and that miR-214 inhibition in osteoblasts may be a potential anabolic strategy for ameliorating osteoporosis., Bone remodeling is delicately regulated by both the number and activity of osteoblasts and osteoclasts (1-3). Osteoblast lineage commitment, proliferation and differentiation are controlled by a well-defined genetic program (2), [...]

Published
2013
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