血管生成
内皮抑素
子宫内膜异位症
PI3K/AKT/mTOR通路
间充质干细胞
癌症研究
体内
蛋白激酶B
医学
内科学
生物
病理
信号转导
细胞生物学
生物技术
作者
Yan Cheng,Qiuyan Guo,Yulei Cheng,Dejun Wang,Liyuan Sun,Tian Liang,Jing Wang,Han Wu,Zhibin Peng,Guangmei Zhang
标识
DOI:10.1093/stcltm/szae079
摘要
Abstract Endometriosis is a chronic inflammatory and neoangiogenic disease. Endostatin is one of the most effective inhibitors of angiogenesis. Mesenchymal stem cells (MSCs) have been investigated as compelling options for cell therapy. However, the effect and mechanism of action of endostatin-expressing endometrial MSCs (EMSCs) in endometriosis are unclear. Here, EMSCs were genetically modified to overexpress endostatin (EMSCs-Endo). A reduction in the angiogenic capacity of HUVECs was observed in vitro after treatment with EMSCs-Endo. EMSCs-Endo significantly suppressed endometriotic lesion growth in vivo. The limited efficacy was associated with suppressed angiogenesis. The miRNA-21-5p level and the levels of p-PI3K, p-mTOR, and p-Akt in HUVECs and mouse endometriotic lesions significantly decreased after treatment with EMSCs-Endo, whereas TIMP3 expression significantly increased. In summary, targeted gene therapy with EMSCs-Endo is feasible, and its efficacy in regulating endometriosis can be attributed to the inhibition of angiogenesis, suggesting that EMSCs could be used as promising vehicles for targeted gene therapy.
科研通智能强力驱动
Strongly Powered by AbleSci AI