2篇
您的检索式：作者名="Moyuan Deng"
|
|
|
题名
|
作者
|
年代
|
出处
|
被引量
|
| 1 | Phosphorylation inhibition of protein-tyrosine phosphatase 1B tyrosine-152 induces bone regeneration coupled with angiogenesis for bone tissue engineering显示文摘A close relationship has been reported to exist between cadherin-mediated cell-cell adhesion and integrin-mediated cell mobility,and protein tyrosine phosphatase 1B(PTP1B)may be involved in maintaining this homeostasis.The stable residence of mesenchymal stem cells(MSCs)and endothelial cells(ECs)in their niches is closely related to the regulation of PTP1B.However,the exact role of the departure of MSCs and ECs from their niches during bone regeneration is largely unknown.Here,we show that the phosphorylation state of PTP1B tyrosine-152(Y152)plays a central role in initiating the departure of these cells from their niches and their subsequent recruitment to bone defects.Based on our previous design of a PTP1B Y152 region-mimicking peptide(152RM)that significantly inhibits the phosphorylation of PTP1B Y152,further investigations revealed that 152RM enhanced cell migration partly via integrinαvβ3 and promoted MSCs osteogenic differentiation partly by inhibiting ATF3.Moreover,152RM induced type H vessels formation by activating Notch signaling.Demineralized bone matrix(DBM)scaffolds were fabricated with mesoporous silica nanoparticles(MSNs),and 152RM was then loaded onto them by electrostatic adsorption.The DBM-MSN/152RM scaffolds were demonstrated to induce bone formation and type H vessels expansion in vivo.In conclusion,our data reveal that 152RM contributes to bone formation by coupling osteogenesis with angiogenesis,which may offer a potential therapeutic strategy for bone defects. | Yong Tang Keyu Luo Yin Chen Yueqi Chen Rui Zhou Can Chen Jiulin Tan Moyuan Deng Qijie Dai Xueke Yu Jian Liu Chengmin Zhang Wenjie Wu Jianzhong Xu Shiwu Dong Fei Luo | 2021 | Bioactive Materials2021，6，7： | 3 |
| 2 | New proangiogenic activity on vascular endothelial cells for C-terminal mechano growth factor显示文摘Angiogenesis 在愈合弯屈是关键的。mechano 生长因素(MGF24E ) 的 C 终端 24-a .a 肽的管理以前被表明了在与控制相比在有缺点的区域附近改革骨头导致更多的血容器。因此,这研究试图决定 MGF24E 是否支持骨头缺点通过增加 MGF24E 的 angiogenesis 愈合并且 MGF24E 是否在 vitro 在 angiogenesis 上有积极效果。angiogenesis 和内在的机制上的 MGF24E 的角色被调查。人的脉管的 endothelial EA.hy926 房间的房间增长,迁居,和 tubulogenesis 与 2% 浆液和 MGF24E 共同对待被决定与脉管的 endothelial 生长因素 165 的 100 ng/ml (VEGF165 ) 比较估计 angiogenesis 积极控制或车辆控制(缓冲磷酸盐盐) 。MGF24E 处理(10 ng/ml ) 显著地与车辆控制相比在 EA.hy926 房间上支持了 angiogenesis 的生物进程。脉管的 endothelial 生长因素和 angiopoietin 的抑制 -- 我由 2% 浆液饥饿的表情被 MGF24E 的 10 ng/ml 的增加在 2% 浆液媒介颠倒。这结果建议 MGF24E 在 angiogenesis 上有保护的效果。而且,分别地,而导致 MGF24 的 tubulogenesis 和 angiogenic 因素表示仅仅部分被禁止,英皇家空军之阶级最低之兵的抑制完全由于 PD98050 预告的处理废除了并且主要堵住了导致 MGF24E 的增长和移植。这些新调查结果建议 MGF24E 由提高包含 MAPK/ERK-signaling 小径的 angiogenic cytokines 的表示支持 angiogenesis。 | Moyuan Deng Yuanliang Wang Bingbing Zhang Peng Liu Hualiang Xiao Jianhua Zhao | 2012 | Acta Biochimica et Biophysica Sinica2012，44，4： | 2 |
您所在的机构暂未开通此部分的功能，请联系管理员