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首页> 外文期刊>Journal of Cellular Physiology >Recombinant non-collagenous domain of alpha2(IV) collagen causes involution of choroidal neovascularization by inducing apoptosis.
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Recombinant non-collagenous domain of alpha2(IV) collagen causes involution of choroidal neovascularization by inducing apoptosis.

机译：重组non-collagenous alpha2域(IV)胶原蛋白导致脉络膜的退化新血管形成,诱导细胞凋亡。

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摘要

Vascular endothelial cells receive proangiogenic or antiangiogenic signals from components of extracellular matrix (ECM) depending upon the situation and many molecular signals can have opposite effects in different vascular beds. Tissue inhibitor of metalloproteinase 1 is antiangiogenic in several tissues, but promotes retinal neovascularization. When cleaved from native collagens, several of the non-collagenous domains (NC1) of basement membrane collagens have antiangiogenic effects in some tissues, but this is context dependent for the NC1 of the alpha 1 chain of collagen IV. It is critical to examine effects in several well-defined model systems before assuming that an ECM component is universally antiangiogenic. In this study, we examined the effects of a recombinant fragment of NC1 of the alpha 2 chain of type IV collagen (alpha2(IV)NC1) in a well-characterized model of ocular neovascularization. Intravitreous or periocular injections of alpha2(IV)NC1 caused selective apoptosis of endothelial cells participating in neovascularization resulting in suppression of neovascularization when the peptide was given prior to onset of new vessel sprouting. Importantly, when the peptide was given after neovascularization had already developed, it caused the new vessels to regress. This suggests that alpha2(IV)NC1, which has previously been shown to suppress tumor angiogenesis in xenograft models, is also a strong antiangiogenic agent in the choroid and is a therapeutic candidate for treatment of neovascular age-related macular degeneration.
机译：血管内皮细胞接收proangiogenic或者从组件的反血管增生的信号细胞外基质(ECM)的根据形势和许多分子信号相反的影响在不同的血管床。的金属蛋白酶组织抑制剂1抗血管新生在几个组织,但促进视网膜新生血管形成。non-collagenous原生胶原蛋白,一些域(NC1)的基底膜胶原蛋白抗血管新生的影响在一些组织中,但这是依赖于上下文的NC1α1链的胶原IV。它是研究的关键影响在一些定义良好的模型系统假设一个ECM组件普遍反血管增生。检查的片段重组的影响NC1 IV型胶原蛋白的α2链(alpha2 (IV) NC1)在一个良好的模型眼部新生血管形成。眼周的注射alpha2 (IV) NC1引起选择性内皮细胞的凋亡参与新血管形成导致抑制新血管形成的时候肽是发病前的新船发芽。新血管形成后已经给出发展,导致新船回归。这表明alpha2 (IV) NC1,之前被证明能够抑制肿瘤血管生成在异种移植模型中,也是一个脉络膜和强烈反血管增生剂治疗治疗候选人新生血管性年龄相关性黄斑变性。

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