G9a 抑制通过阻断 Nox4 介导的氧化应激缓解角膜新生血管化。

G9a Suppression Alleviates Corneal Neovascularization through Blocking Nox4-Mediated Oxidative Stress.

机构信息

Department of Ophthalmology, Renmin Hospital of Wuhan University, Wuhan 430060, China.

出版信息

Oxid Med Cell Longev. 2020 Mar 12;2020:6983268. doi: 10.1155/2020/6983268. eCollection 2020.

BACKGROUND

G9a, a well-known methyltransferase, plays a vital role in biological processes. However, its role in corneal neovascularization (CoNV) remains unclear. and models were assessed in hypoxia-stimulated angiogenesis and in a mouse model of alkali burn-induced CoNV. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions and different reoxygenation times to identify the molecular mechanisms involved in this process.

RESULTS

In this study, we found that G9a was positively related to corneal alkali burn-induced injury. Inhibition of G9a with BIX 01294 (BIX) alleviated corneal injury, including oxidative stress and neovascularization models were assessed in hypoxia-stimulated angiogenesis and in a mouse model of alkali burn-induced CoNV. Human umbilical vein endothelial cells (HUVECs) were cultured under hypoxic conditions and different reoxygenation times to identify the molecular mechanisms involved in this process.

背景

G9a 是一种众所周知的甲基转移酶，在生物过程中发挥着重要作用。然而，它在角膜新生血管化（CoNV）中的作用尚不清楚。本研究通过缺氧刺激血管生成和碱性烧伤诱导 CoNV 的小鼠模型评估了 G9a 的作用。在缺氧条件下和不同复氧时间培养人脐静脉内皮细胞（HUVEC），以确定该过程涉及的分子机制。

结果

本研究发现 G9a 与角膜碱性烧伤诱导的损伤呈正相关。用 BIX 01294（BIX）抑制 G9a 可减轻角膜损伤，包括氧化应激和新生血管形成。本研究通过缺氧刺激血管生成和碱性烧伤诱导 CoNV 的小鼠模型评估了 G9a 的作用。在缺氧条件下和不同复氧时间培养人脐静脉内皮细胞（HUVEC），以确定该过程涉及的分子机制。