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ANGPTL4通过内皮 - 介质细胞过渡促进胆道新血管化和亚皮纤维化

Jia Chen^1,2, Ying Yang^2,3, Shu Su^1,2

¹Suzhou Medical College of Soochow University, Suzhou, 215123, China.

International ophthalmology

|November 25, 2024

概括

血管类4 (ANGPTL4) 通过诱导内皮细胞-介质细胞过渡 (EndMT) 来促进胆管新血管化和纤维化. 抑制ANGPTL4可能为与年龄相关的黄斑变性提供一种新的治疗策略.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
遗传学是一个遗传学.

背景情况:

与年龄相关的黄斑变性 (AMD) 是导致视力丧失的主要原因.
状新血管化 (CNV) 和亚皮纤维化是新血管AMD (nAMD) 的关键病理特征.
CNV和纤维化背后的分子机制需要进一步阐明.

研究的目的:

为了研究ANGPTL4在CNV和子纤维化病变发生过程中的作用.
探索ANGPTL4作为nAMD治疗点的潜力.

主要方法:

对nAMD中差异表达基因的GEO数据库的生物信息分析.
建立和验证激光诱导的CNV小鼠模型.
在体外研究中使用TGF-β2诱导的人类静脉内皮细胞 (HUVEC) 来建模EndMT.
在体外和体内使用小干扰RNA (siRNA) 降低ANGPTL4.
评估CNV和纤维化使用 fundus光素血管学 (FFA),光学连贯性断层扫描血管学 (OCTA) 和免疫光染色.

主要成果:

在CNV小鼠模型和TGF-β2诱导的EndMT中,ANGPTL4表达显著上调.
ANGPTL4的淘汰抑制了EndMT,细胞迁移和在体外的入侵.
通过抑制EndMT,ANGPTL4 Knockdown减少了体内中枢神经瘤的形成和子皮膜纤维化.

结论:

ANGPTL4促进中枢神经瘤和亚纤维化,可能是通过诱导EndMT.
ANGPTL4代表了对nAMD的一个潜在的新疗法标.

关键词:

ANGPTL4 在线观看冠状腺新血管化疗法内皮细胞 - 介质细胞过渡亚视网膜纤维化是什么

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