氧化轻密度脂蛋白（ox-LDL）引起内皮功能障碍，这是动脉粥样硬化形成的重要决定因素，并随后导致细胞凋亡。动脉粥样硬化是威胁人类健康并导致全球死亡的最重要的心血管疾病（CVD）之一。最近，长非编码 RNA (lncRNA) 被认为参与血管生物学。 Ox-LDL 激活核因子 kappa-B (NF-κB)，NF-κB 相互作用 lncRNA (NKILA) 抑制 NF-κB 信号传导。在这项研究中，假设 NKILA 可能调节内皮细胞 (EC) 凋亡，因此在动脉粥样硬化的发病机制中发挥作用。这一假设基于 EC 细胞凋亡有助于动脉粥样硬化的发展以及 NKILA 已成为 CVD 中重要的 lncRNA 的知识。 Bcl-2 相关 X 蛋白 (BAX)、半胱天冬酶 9 (CASP9)、细胞色素 c (Cyt c、CYCS)、凋亡蛋白酶激活因子 1 (APAF1) 和 B 细胞淋巴瘤 2 (BCL-2) 基因的表达使用定量逆转录聚合酶链反应 (RT-qPCR) 对经 ox-LDL 处理并转染 NKILA siRNA 的人脐静脉内皮细胞 (HUVEC) 进行分析。 BAX、CASP9、CYCS、APAF1 和 BCL-2 基因表达在 ox-LDL 和 NKILA siRNA 处理的 HUVEC 中下调。此外，当NKILA基因表达的阈值/定量循环（Cq）值增加时，BAX、CASP9、APAF1和BCL-2基因表达的Cq值显着增加。 NKILA 基因沉默导致的所有这些基因的表达检测可能为动脉粥样硬化中 EC 凋亡的表观遗传学研究提供指导。©2024 Bayyurt 等人。

Oxidized light-density lipoprotein (ox-LDL) causes endothelial dysfunction, which is an important determinant of atherogenesis, and subsequently leads to apoptosis. Atherosclerosis is one of the most significant cardiovascular diseases (CVDs) threatening human health and causes death worldwide. Recently, long noncoding RNAs (lncRNAs) have been suggested to involved in vascular biology. Ox-LDL activates nuclear factor kappa-B (NF-κB), and NF-κB interacting lncRNA (NKILA) inhibits NF-κB signaling. In this study, the hypothesis is that NKILA may regulate endothelial cell (EC) apoptosis and, therefore, play a role in the pathogenesis of atherosclerosis. This hypothesis is based on the knowledge that EC apoptosis contributes to atherosclerosis development and that NKILA has become a prominent lncRNA in CVDs. The expression of Bcl-2-associated X protein (BAX), caspase 9 (CASP9), cytochrome c (Cyt c, CYCS), apoptotic protease activating factor 1 (APAF1), and B-cell lymphoma 2 (BCL-2) genes in human umbilical vein endothelial cells (HUVEC) treated with ox-LDL and transfected with NKILA siRNA was analyzed using quantitative reverse transcription polymerase chain reaction (RT-qPCR). BAX, CASP9, CYCS, APAF1, and BCL-2 gene expression was downregulated in ox-LDL and NKILA siRNA-treated HUVEC. In addition, when threshold/quantification cycle (Cq) values of NKILA gene expression increased, Cq values of BAX, CASP9, APAF1, and BCL-2 gene expression increased statistics significantly. The expression detection of all these genes, resulting from NKILA gene silencing, may provide guidance for epigenetic studies on EC apoptosis in atherosclerosis.©2024 Bayyurt et al.