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您的检索式：作者名="Yuteng Weng"
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| 1 | A novel lineage of osteoprogenitor cells with dual epithelial and mesenchymal properties govern maxillofacial bone homeostasis and regeneration after MSFL显示文摘Bone regeneration originates from proliferation and differentiation of osteoprogenitors via either endochondral or intramembranous ossifcation;and the regeneration capacities decline with age and estrogen loss.Maillary sinus floor lifting(MSFL)is a commonly used surgical procedure for guiding bone regeneration in mailla.Radiographic analysis of 1210 clinical cases of maxilla bone regeneration after MSFL revealed that the intrasinus osteogenic eficacy was independent of age and gender,however;and this might be related to the Schneiderian membrane that lines the sinus cavity.In view of the particularity of this biological process,our present study aimed to elucidate the underlying mechanism of MSFL-induced bone regeneration.We frst established a murine model to simulate the clinical MSFL.By single cell RNA-sequencing and flow cytometry-based bulk RNA-sequencing,we identifed a novel Krt14^(+)Ctsk^(+)subset of cells that display both epithelial and mesenchymal properties and the transcriptomic feature of osteoprogenitors.Dual recombinases-mediated lineage tracing and oss-offunction analyses showed that these Krt14^(+)Ctsk^(+)progenitors contribute to both MSFL-induced osteogenesis and physiological bone homeostasis by differentiating into Krt14 Ctsk^(+)descendants which show robust osteogenic capacity.In addition,we detected a similar population of Kt14^(+)Ctsk^(+)cells in human samples of Schneiderian membrane,which show a highly similar osteogenic potential and transcriptomic feature to the corresponding cells in mice.The identifcation of this Krt14^(+)Ctsk^(+)population,featured by osteoprogenitor charateristics and dual epithelial-mesenchymal properties,provides new insight into the understanding of bone regeneration and may open more possibilities for clinical applications. | Yuteng Weng Haicheng Wang Di Wu Shuyu Xu Xiaofan Chen Jie Huang Yanhuizhi Feng Lin Li Zuolin Wang | 2022 | Cell Research2022，32，9： | 5 |
| 2 | Glycosylation of dentin matrix protein 1 is a novel key element for astrocyte maturation and BBB integrity显示文摘血大脑障碍(BBB ) 是在 endothelial 房间和星形细胞之间形成的一条紧密的边界,它在循环把大脑与大多数病原体以及神经毒素分开并且保护。然而,详细说明了涉及 BBB 的形成的分子的播放器完全不被知道。牙质矩阵蛋白质 1 (DMP1 )-proteoglycan (PG ) 被知道涉及骨头和牙质的矿化作用,也与未知功能包括大脑在软纸巾被表示。在现在的学习,我们报导 DMP1-PG 在大脑星形细胞被表示并且在 BBB 充实单位。DMP1 的唯一的 glycosylation 地点在在鼠标的蛋白质的 N 终端域是 serine89 (S89 ) 。有 DMP1 的变异的老鼠削尖把 S89 改变到 glycine (S89G ) 的变化,它蛋白质的完全根除的 glycosylation,表明的严重 BBB 混乱。DMP1 变异的鼠标的另一个品种,缺乏 DMP1 的 C 终端域,表明了正常 BBB 功能。S89G-DMP1 星形细胞的极性被破坏,房间房间粘附被松开。通过一组分析,我们发现 DMP1 glycosylation 极其在 vitro 并且在 vivo 为星形细胞成熟被要求。S89G-DMP1 变异的星形细胞没能表示 aquaporin 4 并且减少了 laminin 和 ZO1 表示,它导致了 BBB 的混乱。有趣地,在 nestin 倡导者驾驶的老鼠大脑的野类型的 DMP1-PG 的 overexpression 在野类型层次以外提高了 laminin 和 ZO1 表示并且能有效地抵抗的静脉内的导致甘露糖醇的 BBB 可逆的洞。一起拿,我们的学习不仅揭示了一个新奇元素,即, DMP1-PG,调整了 BBB 形成,而且把新功能分到 DMP1-PG。 | Bo Jing Chunxue Zhang Xianjun Liu Liqiang Zhou Jiping Liu Yinan Yao Juehua Yu Yuteng Weng Min Pan Jie Liu Zuolin Wang Yao Sun Yi Eve Sun | 2018 | Protein & Cell2018，9，3： | 5 |
| 3 | Glycosylation of dentin matrix protein 1 is critical for fracture healing via promoting chondrogenesis显示文摘Fractures are frequently occurring diseases that endanger human health. Crucial to fracture healing is cartilage formation, which provides a bone-regeneration environment. Cartilage consists of both chondrocytes and extracellular matrix (ECM). The ECM of cartilage includes collagens and various types of proteoglycans (PGs), which play important roles in maintaining primary stability in fracture healing. The PG form of dentin matrix protein 1 (DMP1-PG) is involved in maintaining the health of articular cartilage and bone. Our previous data have shown that DMP1-PG is richly expressed in the cartilaginous calluses of fracture sites. However, the possible significant role of DMP1-PG in chondrogenesis and fracture healing is unknown. To further detect the potential role of DMP1-PG in fracture repair, we established a mouse fracture model by using a glycosylation site mutant DMP1 mouse (S89G-DMP1 mouse). Upon inspection, fewer cartilaginous calluses and down-regulated expression levels of chondrogenesis genes were observed in the fracture sites of S89G-DMP1 mice. Given the deficiency of DMP1-PG, the impaired IL-6/JAK/STAT signaling pathway was observed to affect the chondrogenesis of fracture healing. Overall, these results suggest that DMP1-PG is an indispensable proteoglycan in chondrogenesis during fracture healing. | Hui Xue Dike Tao Yuteng Weng Qiqi Fan Shuang Zhou Ruilin Zhang Han Zhang Rui Yue Xiaogang Wang Zuolin Wang Yao Sun | 2019 | Frontiers of Medicine2019，13，5： | 2 |
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