DCZ3301, an aryl-guanidino agent, inhibits ocular neovascularization via PI3K/AKT and ERK1/2 signaling pathways
文献类型：期刊论文
| 作者 | Xu, Kai2,3; Li, Bo1,4; Zhang, Shujie2,3; Hu, Fangyuan2,3; Xu, Zhijian1,4 ; Li, Lei2,3; Zhang, Yihan2,3; Zhu, Weiliang1,4; Zhao, Chen2,3
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| 刊名 | EXPERIMENTAL EYE RESEARCH
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| 出版日期 | 2020-12-01 |
| 卷号 | 201页码:8 |
| 关键词 | DCZ3301 Apoptosis PI3K/AKT pathway ERK1/2 pathway Choroid microvascular sprouting Corneal neovascularization |
| ISSN号 | 0014-4835 |
| DOI | 10.1016/j.exer.2020.108267 |
| 通讯作者 | Zhu, Weiliang(wlzhu@simm.ac.cn) ; Zhao, Chen(dr_zhaochen@163.com) |
| 英文摘要 | Neovascularization is a critical process in the pathophysiology of neovascular eye diseases. Although anti-VEGF therapy has achieved remarkable curative effects, complications, limited efficacy and drug resistance remain the prominent problems. DCZ3301, an aryl-guanidino compound, was reported to have anti-tumor activity in the previous studies. Here, we demonstrated the effects of DCZ3301 on human umbilical vein endothelial cell (HUVEC) in vitro, and performed choroid microvascular sprouting assay ex vivo and alkali-burn induced corneal neovascularization mouse model in vivo. We found that DCZ3301 inhibited the proliferation, migration, and tube formation of HUVECs, while inducing the spontaneous apoptosis of HUVECs by suppressing the activation of PI3K/AKT and ERK1/2 pathways. Furthermore, DCZ3301 inhibited the choroid microvascular sprouting, diminished the area of corneal neovascularization and attenuated the edema of corneal stroma after alkali burn. Together, these results suggested that DCZ3301 exerted anti-angiogenic properties, and might be regarded as a potential candidate for ocular neovascularization. |
| WOS关键词 | THERAPY ; ANGIOGENESIS ; MECHANISMS ; CLEAVAGE ; GROWTH |
| 资助项目 | National Natural Science Foundation of China[81525006] ; National Natural Science Foundation of China[81670864] ; National Natural Science Foundation of China[81730025] ; Shanghai Outstanding Academic Leaders[2017BR013] ; Excellent Academic Leaders of Shanghai[18XD1401000] ; National Key RD Plan[2016YFA0502301] ; National Science & Technology Major Project Key New Drug Creation and Manufacturing Program, China[2018ZX09711002] |
| WOS研究方向 | Ophthalmology |
| 语种 | 英语 |
| WOS记录号 | WOS:000601048900005 |
| 出版者 | ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/296345]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Zhu, Weiliang; Zhao, Chen |
| 作者单位 | 1.Chinese Acad Sci, CAS Key Lab Receptor Res, Shanghai, Peoples R China 2.Fudan Univ, Chinese Acad Med Sci, NHC Key Lab Myopia, Eye Inst,Eye & ENT Hosp,Shanghai Med Coll,Key Lab, Shanghai, Peoples R China 3.Fudan Univ, Shanghai Key Lab Visual Impairment & Restorat, Shanghai, Peoples R China 4.Chinese Acad Sci, Shanghai Inst Mat Med, Drug Discovery & Design Ctr, Shanghai, Peoples R China |
| 推荐引用方式 GB/T 7714 | Xu, Kai,Li, Bo,Zhang, Shujie,et al. DCZ3301, an aryl-guanidino agent, inhibits ocular neovascularization via PI3K/AKT and ERK1/2 signaling pathways[J]. EXPERIMENTAL EYE RESEARCH,2020,201:8. |
| APA | Xu, Kai.,Li, Bo.,Zhang, Shujie.,Hu, Fangyuan.,Xu, Zhijian.,...&Zhao, Chen.(2020).DCZ3301, an aryl-guanidino agent, inhibits ocular neovascularization via PI3K/AKT and ERK1/2 signaling pathways.EXPERIMENTAL EYE RESEARCH,201,8. |
| MLA | Xu, Kai,et al."DCZ3301, an aryl-guanidino agent, inhibits ocular neovascularization via PI3K/AKT and ERK1/2 signaling pathways".EXPERIMENTAL EYE RESEARCH 201(2020):8. |
入库方式： OAI收割
来源：上海药物研究所
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