Fibulin-7 C-terminal fragment and its active synthetic peptide suppress choroidal and retinal neovascularization
Fibulin-7 C-terminal fragment and its active synthetic peptide suppress choroidal and retinal neovascularization
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DOI：
10.1016/j.mvr.2020.103986
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发表时间：
2020-05-01
影响因子：
3.1
通讯作者：
Yamada, Yoshihiko
中科院分区：
文献类型：
--
作者：
Ikeuchi, Tomoko;Kanan, Yogita;Yamada, Yoshihiko
湿性年龄相关性黄斑变性（AMD）和糖尿病视网膜病变是通过增加血管生成导致失明的主要原因。尽管VEGF中和蛋白提供了益处，但不一致的反应表明需要新的疗法。我们先前鉴定了Fibulin-7 C-末端片段（Fbln 7-C）作为体外血管生成抑制剂。在这里，我们表明Fbln 7-C在涉及脉络膜新生血管（CNV）的湿性AMD和涉及氧诱导的缺血性视网膜病变的糖尿病视网膜病变的模型中抑制体内新生血管形成。此外，来自Fbln 7-C的短肽序列负责Fbln 7-C的抗血管生成性质。我们的工作表明Fbln 7-C作为湿性AMD和缺血性视网膜病变的治疗候选者。
Wet age-related macular degeneration (AMD) and diabetic retinopathy are the leading causes of blindness through increased angiogenesis. Although VEGF-neutralizing proteins provide benefit, inconsistent responses indicate a need for new therapies. We previously identified the Fibulin-7 C-terminal fragment (Fbln7-C) as an angiogenesis inhibitor in vitro. Here we show that Fbln7-C inhibits neovascularization in vivo, in both a model of wet AMD involving choroidal neovascularization (CNV) and diabetic retinopathy involving oxygen-induced ischemic retinopathy. Furthermore, a short peptide sequence from Fbln7-C is responsible for the anti-angiogenic properties of Fbln7-C. Our work suggests Fbln7-C as a therapeutic candidate for wet AMD and ischemic retinopathy.