The roles of some long non-coding RNAs (lncRNAs) in intracranial aneurysm (IA) have been investigated in many studies. The aim of this study is to elucidate the mechanism of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1)/microRNA-143 (miR-143)/vascular endothelial growth factor-A (VEGFA) signal axis in vascular endothelial injury-induced IA. MALAT1, miR-143, and VEGFA expression in IA tissues and normal arterial tissues were detected. Matrix metalloproteinase 9 (MMP-9) in tissues, von Willebrand factor (vWF) in serum and tissues, and endothelin-1 (ET-1) in serum were detected. The modeled IA rats were injected with silenced or overexpressed MALAT1 for detecting vascular endothelial injury. Vascular endothelial cells from patients with IA were abstracted and transfected with silenced or overexpressed MALAT1 to verify the impacts of MALAT1 on cell viability and apoptosis. The connections among MALAT1, miR-143, and VEGFA were verified by online prediction, luciferase activity, and RNA-pull down assays. Overexpression of MALAT1 and VEGFA and poor expression of miR-143 were found in IA tissues. Downregulation of MALAT1 inhibited blood pressure, the expression of ET-1, vWF, and MMP-9, as well as the apoptotic index of vascular endothelial cells of rats with IA. Downregulated MALAT1 inhibited apoptosis and promoted viability of vascular endothelial cells in IA. MALAT1 bound to miR-143 and miR-143 targeted VEGFA. This study suggests that MALAT1 elevates VEGFA expression through competitive binding to miR-143, thereby boosting apoptosis and attenuating viability of vascular endothelial cells in IA.

许多研究已经研究了一些长链非编码 RNA (lncRNA) 在颅内动脉瘤 (IA) 中的作用。本研究的目的是阐明lncRNA转移相关肺腺癌转录物1（MALAT1）/microRNA-143（miR-143）/血管内皮生长因子-A（VEGFA）信号轴在血管内皮损伤诱导的IA中的机制。检测IA组织和正常动脉组织中MALAT1、miR-143和VEGFA的表达。检测组织中基质金属蛋白酶9（MMP-9）、血清和组织中血管性血友病因子（vWF）以及血清中内皮素-1（ET-1）。给模型IA大鼠注射沉默或过表达的MALAT1以检测血管内皮损伤。提取 IA 患者的血管内皮细胞并用沉默或过表达的 MALAT1 转染，以验证 MALAT1 对细胞活力和凋亡的影响。MALAT1、miR-143 和 VEGFA 之间的联系通过在线预测、荧光素酶活性和 RNA 下拉测定进行验证。在 IA 组织中发现 MALAT1 和 VEGFA 过表达，而 miR-143 低表达。MALAT1的下调可抑制IA大鼠的血压、ET-1、vWF和MMP-9的表达以及血管内皮细胞的凋亡指数。下调 MALAT1 可抑制 IA 中血管内皮细胞的凋亡并促进其活力。MALAT1 与 miR-143 结合，并且 miR-143 靶向 VEGFA。这项研究表明 MALAT1 通过与 miR-143 竞争性结合来提高 VEGFA 表达，