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正常角膜中血管内皮生长因子(VEGFs)和血小板衍生生长因子(PDGFs)的基因表达谱。

Gene Expression Profile of Vascular Endothelial Growth Factors (VEGFs) and Platelet-derived Growth Factors (PDGFs) in the Normal Cornea.

机构信息

Department IX, Surgery I/Ophthalmology, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania.

Department of Microscopic Morphology/Histology, Victor Babes University of Medicine and Pharmacy, Timisoara, Romania.

出版信息

In Vivo. 2021 Mar-Apr;35(2):805-813. doi: 10.21873/invivo.12321.

Abstract

BACKGROUND/AIM: Angiogenic growth factors expression is not known in the normal cornea. The aim was to study corneal gene expression profile of VEGF and PDGF pathways influencing the avascular state of cornea.

MATERIALS AND METHODS

cDNA synthesis was performed from mRNA extracted from five fresh pig corneas followed by cDNA synthesis and analysis of VEGF and PDGF pathways by TaqMan Array gene expression profile.

RESULTS

Normal pig cornea lacks VEGFR2 and VEGFR3 gene expression. MK2 and AKT1 genes were significantly overexpressed (p=0.000684, p=0.050995, respectively). Six PDGF pathway genes were overexpressed: TIAM1 (p=0.047), PIK3CA (p=0.00005), IKBKG (p=0.000006), PAK4 (p=0.034), RAC1 (p=0.000006 and PTGS2, p=0.00375). PDGF A was up-regulated, but not with a statistical significance (p=0.79911), while PDGFRα was down-regulated and PDGFRβ was not expressed.

CONCLUSION

Normal cornea avascularity is given by growth factor receptors down-regulation. Rapid corneal neovascularisation is induced by activation of the main angiogenic growth factors that induce angiogenic cascade and vessel recruitment.

摘要

背景/目的:血管生成生长因子的表达在正常角膜中尚不清楚。本研究旨在研究影响角膜无血管状态的 VEGF 和 PDGF 通路的角膜基因表达谱。

材料和方法

从 5 个新鲜猪眼角膜中提取 mRNA 后进行 cDNA 合成,然后通过 TaqMan 基因表达谱分析 VEGF 和 PDGF 通路。

结果

正常猪眼角膜缺乏 VEGFR2 和 VEGFR3 基因表达。MK2 和 AKT1 基因表达显著上调(p=0.000684,p=0.050995)。6 个 PDGF 通路基因过表达:TIAM1(p=0.047)、PIK3CA(p=0.00005)、IKBKG(p=0.000006)、PAK4(p=0.034)、RAC1(p=0.000006)和 PTGS2(p=0.00375)。PDGF A 上调,但无统计学意义(p=0.79911),而 PDGFRα 下调,PDGFRβ 不表达。

结论

正常角膜无血管性是由生长因子受体下调引起的。角膜新生血管的快速发生是由主要血管生成生长因子的激活引起的,这些因子诱导血管生成级联和血管募集。

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