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抑制LncRNA MALAT1抑制胆道新血管化的发展

Xiaoli Zhang¹, Shu Du², Defeng Yang³

¹Changchun Aier Eye Hospital, Aier Eye Hospital Group, Changchun, Nanguang District, Jilin Province, China.

|October 9, 2023

概括

与转移相关的肺腺癌转录1 (MALAT1) 在与年龄相关的黄斑退化中被上调. 抑制MALAT1可降低冠状腺新血管化 (CNV),并可能为CNV提供新的治疗点.

科学领域:

眼科医生眼科眼科
分子生物学分子生物学
遗传学遗传学是一个

背景情况:

长非编码RNAs (lncRNAs) 是与年龄相关的黄斑变性 (AMD) 病变发生的关键调节者.
转移相关的肺腺癌转录1 (MALAT1) 涉及各种细胞过程.

研究的目的:

调查MALAT1在胆道新血管化 (CNV) 进展中的作用.
阐明MALAT1在CNV病变发生过程中的潜在分子机制.

主要方法:

在体内 (激光诱导的小鼠CNV模型) 和体外 (暴露于低氧的人体胆道血管内皮细胞) 的CNV模型中建立.
利用小干扰RNA (siRNA) 来降低MALAT1表达在体内和体外.
分析了MALAT1表达,CNV发育,泄漏,细胞增殖,迁移和管道形成.

主要成果:

在视网膜色素上皮质 - 冠状体复合体中,MALAT1的表达显著上调.
在体内,MALAT1倒置抑制了中枢神经瘤的发育和泄漏.
在试管体内,MALAT1 Knockdown 降低了人体冠状血管内皮细胞的增殖,迁移和管道形成.
MALAT1作为一个miR-17-5p海绵,调节血管内皮生长因子A (VEGFA) 和E26转化特异-1 (ETS1) 表达.

结论:

马拉特1在CNV的发病过程中起着至关重要的作用.
马拉特1/miR-17-5p/VEGFA或ETS1轴代表了潜在的治疗瘤治疗的目标.

关键词:

冠状腺新血管化 (CNV)人体冠状血管内皮细胞 (HCVECs)氧气过低是因为缺氧.转移相关的肺腺癌转录1 (MALAT1)

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