微泡
细胞生物学
间质细胞
蛋白激酶B
Wnt信号通路
外体
信号转导
PI3K/AKT/mTOR通路
旁分泌信号
血管生成
癌症研究
化学
小RNA
生物
生物化学
基因
受体
作者
Lu Liu,Yaqin Liu,Chun Feng,Jiang Chang,Runqing Fu,Tingting Wu,Fei Yu,Xiaoting Wang,Lunguo Xia,Chengtie Wu,Bing Fang
出处
期刊:Biomaterials
[Elsevier]
日期:2018-11-08
卷期号:192: 523-536
被引量:135
标识
DOI:10.1016/j.biomaterials.2018.11.007
摘要
The chemical signals of biomaterials could influence bone marrow stromal cells (BMSCs)-endothelial cells (ECs) communication during vascularized bone regeneration. However, the underlying mechanisms still remain unknown. Exosomes, a series of extracellular vesicles, have recently emerged as potential paracrine mediators in cell-cell communication. However, whether exosomes and exosomal microRNAs (miRNAs) are involved in the chemical signals of biomaterials-modulated BMSCs-ECs communication are unknown. Hence, in the present study, a model Li-incorporated bioactive glass ceramic (Li-BGC) was applied to explore the chemical signals of biomaterials mediated cell-cell communication between BMSCs and ECs. Our results showed that Li-BGC directly promoted the pro-angiogenic capability of HUVECs in vitro and new blood vessel ingrowth in vivo. Moreover, Li-BGC activated Wnt/β-catenin, AKT and NF-κB signaling pathways, while AKT signaling pathway might function as the upstream of Wnt/β-catenin and NF-κB signaling pathways. More importantly, Li-BGC further facilitated the pro-angiogenic capacity of HUVECs by eliciting the expression of exosomal pro-angiogenic miR-130a in BMSCs-derived exosomes, which subsequently leading to the downregulation of PTEN protein and activation of AKT pathway, ultimately resulting in the elevated proliferation, migration and tube formation of endothelial cells, as well as the upregulated expression of pro-angiogenic genes. Our findings may provide new insights into the regulatory roles of the chemical signals of biomaterials in BMSCs-ECs communication via stimulating exosomal miR-130a secretion and PTEN/AKT signaling pathway in the angiogenic process of bone remodelling.
科研通智能强力驱动
Strongly Powered by AbleSci AI