Purpose

To evaluate the role of Toll-like receptor 2 (TLR2) signaling in retinal neovascularization in a mouse model of oxygen-induced retinopathy (OIR).

Materials and methods

The OIR model was established in C57BL/6J wild type (WT) mice and TLR2^−/− mice. Retinal neovascularization in the OIR model was measured by counting new vascular cell nuclei above the internal limiting membrane and analyzing flat-mounted retinas perfused with fluorescein dextran and immunostained with Griffonia Simplicifolia (GS) isolectin. The expression of TLR2 and VEGF in the retina was detected by immunofluorescence. Expression of TGF- β1, b-FGF, and IL-6 mRNA in the retina was measured by quantitative real-time PCR.

Results

Compared to WT OIR mice, retinal neovascularization was attenuated in TLR2^−/− OIR mice. The co-expressions of TLR2 and VEGF were remarkably and consistently increased in WT OIR mice; however, there was no expression of TLR2 and a significant decrease in VEGF expression in TLR2^−/− OIR mice. These results suggest that TLR2 plays a central role in OIR model angiogenesis. Expression of TGF- β1, b-FGF, and IL-6 mRNA were reduced in the TLR2^−/− OIR mice, suggesting that the inflammatory response induced by TLR2 relates to angiogenesis.

Conclusion

TLR2 signaling in the retina is associated with neovascularization in mice. Inflammation contributes to the activation of angiogenesis and is partially mediated through the TLR2-VEGF retinal signaling pathway.

中文翻译：

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TLR2 信号有助于氧诱导视网膜病变的血管生成

目的

评估 Toll 样受体 2 (TLR2) 信号在氧诱导视网膜病变 (OIR) 小鼠模型中视网膜新生血管形成中的作用。

材料和方法

在 C57BL/6J 野生型 (WT) 小鼠和 TLR2 ^-/-小鼠中建立 OIR 模型。OIR 模型中的视网膜新生血管形成是通过计算内界膜上方的新血管细胞核并分析用荧光素葡聚糖灌注并用 Griffonia Simplicifolia (GS) isolectin 免疫染色的平装视网膜来测量的。免疫荧光法检测视网膜中TLR2和VEGF的表达。通过实时定量 PCR 测量视网膜中 TGF-β1、b-FGF 和 IL-6 mRNA 的表达。

结果

与WT OIR小鼠相比，TLR2 ^-/- OIR小鼠的视网膜新生血管形成减弱。TLR2和VEGF的共表达在WT OIR小鼠中显着且持续增加；然而，在 TLR2 ^-/- OIR 小鼠中没有 TLR2 表达并且 VEGF 表达显着降低。这些结果表明 TLR2 在 OIR 模型血管生成中起着核心作用。TLR2 ^-/- OIR 小鼠中 TGF-β1、b-FGF 和 IL-6 mRNA 的表达降低，表明 TLR2 诱导的炎症反应与血管生成有关。

结论

视网膜中的 TLR2 信号传导与小鼠的新生血管形成有关。炎症有助于血管生成的激活，部分通过 TLR2-VEGF 视网膜信号通路介导。