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首页> 外文期刊>Journal of Cellular Physiology >Angiopoietin 2 expression in the retina: upregulation during physiologic and pathologic neovascularization.
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Angiopoietin 2 expression in the retina: upregulation during physiologic and pathologic neovascularization.

机译:检验2表达在视网膜上:upregulation在生理和病理新生血管形成。

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摘要

Vascular development in the embryo requires coordinated signaling through several endothelial cell-specific receptors; however, it is not known whether this is also required later during retinal vascular development or as part of retinal neovascularization in adults. The Tie2 receptor has been implicated in stabilization and maturation of vessels through action of an agonist ligand, angiopoietin 1 (Ang1) and an antagonistic ligand, Ang2. In this study, we have demonstrated that ang2 mRNA levels are increased in the retina during development of the deep retinal capillaries by angiogenesis and during pathologic angiogenesis in a model of ischemic retinopathy. Mice with hemizygous disruption of the ang2 gene by insertion of a promoterless beta-galactosidase (beta gal) gene behind the ang2 promoter, show constitutive beta gal staining primarily in cells along the outer border of the inner nuclear layer identified as horizontal cells by colocalization of calbindin. During development of the deep capillary bed or retinal neovascularization, other cells in the inner nuclear layer and ganglion cell layer, in regions of neovascularization, stain for beta gal. Thus, there is temporal and spatial correlation of Ang2 expression with developmental and pathologic angiogenesis in the retina, suggesting that it may play a role. Copyright 2000 Wiley-Liss, Inc.
机译:胚胎血管发展的需要协调信号通过几个内皮特异性受体;是否还需要以后期间视网膜血管发展的一部分成人视网膜新生血管形成。已经与稳定和受体通过行动的一个成熟的船只受体激动剂配体,检验1 (Ang1)和一个敌对的配体,Ang2。证明ang2 mRNA水平增加在视网膜的发展深视网膜毛细血管的血管生成和期间病理性血管生成在缺血性的典范视网膜病变。通过插入promoterless ang2基因苷酶(β加)背后的基因ang2启动子,显示本构β加染色主要在细胞外确认为边界内的核层水平细胞colocalization calbindin。在深毛细血管床或发展视网膜新生血管形成,其他细胞内部核层和神经节细胞层地区的新血管形成,β的污点加。因此,有时间和空间Ang2表达式与发育的相关性和病理性血管生成在视网膜上,这表明它可能扮演一个角色。2000 Wiley-Liss, Inc。

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