Li Ming-Peng, Hao Zi-Chen, Yan Meng-Qi, Xia Chun-Li, Wang Zhong-Hua, Feng Ying-Qing
The Second School of Clinical Medicine, Southern Medical University, Guangzhou, China.
Department of Cardiology, Guangdong Cardiovascular Institute, Guangdong Provincial People's Hospital, Guangdong Academy of Medical Sciences, Guangzhou, China.
Ann Transl Med. 2022 Mar;10(6):286. doi: 10.21037/atm-22-507.
Atherosclerosis is the most common cause of cardiovascular disease, accompanied by high mortality and poor prognosis. Low-density lipoprotein (LDL) and its oxidized form oxidized low-density lipoprotein (oxLDL) play an important role in atherosclerosis. This article will explore the role of the lncRNA (colorectal cancer associated 1)// (secreted phosphoprotein 1) pathway in oxLDL in causing human coronary artery endothelial cells (HCAECs) inflammation and related biological function changes.
OxLDL was used to stimulate HCAECs. The inflammatory response and biological function changes of HCAECs were analyzed, total RNA-seq was performed on HCAECs before and after stimulation, and RT-Qpcr (real-time quantitative PCR) was used to verify the differential genes. Interference of the expression of in HCAECs was performed by siRNA interference technology to verify the role of in the biological function changes of HCAECs after oxLDL stimulation, and further prove that affects through .
OxLDL can affect the oxidative stress response of HCAECs, which in turn affects the apoptosis and wound healing ability of HCAECs. and were highly expressed after oxLDL stimulation, while was the opposite. After interference, the oxidative stress level of HCAECs stimulated by oxLDL decreased, the apoptosis level also significantly decreased, and the wound healing ability was enhanced. After simultaneous interference and recovery of the expression of , these improved functions disappeared. The dual-luciferase assay confirmed that and , and has binding targets.
OxLDL can up-regulate the expression of in HCAECs, which in turn affects the intracellular pathway to regulate the level of oxidative stress in cells. This in turn affects the level of apoptosis and wound healing ability, which causes cells to produce a continuous inflammatory response.
动脉粥样硬化是心血管疾病最常见的病因，死亡率高且预后不良。低密度脂蛋白（LDL）及其氧化形式氧化型低密度脂蛋白（oxLDL）在动脉粥样硬化中起重要作用。本文将探讨长链非编码RNA（lncRNA）（结直肠癌相关1）//（分泌型磷蛋白1）途径在oxLDL导致人冠状动脉内皮细胞（HCAECs）炎症及相关生物学功能变化中的作用。
用oxLDL刺激HCAECs。分析HCAECs的炎症反应和生物学功能变化，对刺激前后的HCAECs进行全转录组测序，并采用实时定量聚合酶链反应（RT-Qpcr）验证差异基因。通过小干扰RNA（siRNA）干扰技术干扰HCAECs中lncRNA的表达，以验证lncRNA在oxLDL刺激后HCAECs生物学功能变化中的作用，并进一步证明lncRNA通过lncRNA（结直肠癌相关1）影响lncRNA（分泌型磷蛋白1）。
oxLDL可影响HCAECs的氧化应激反应，进而影响HCAECs的凋亡和伤口愈合能力。oxLDL刺激后lncRNA（结直肠癌相关1）和lncRNA（分泌型磷蛋白1）高表达，而lncRNA（lncRNA（结直肠癌相关1））则相反。lncRNA（lncRNA（结直肠癌相关1））干扰后，oxLDL刺激的HCAECs氧化应激水平降低，凋亡水平也显著降低，伤口愈合能力增强。lncRNA（lncRNA（结直肠癌相关1））干扰并恢复lncRNA（分泌型磷蛋白1）表达后，这些改善的功能消失。双荧光素酶报告基因检测证实lncRNA（结直肠癌相关1）与lncRNA（lncRNA（结直肠癌相关1））、lncRNA（分泌型磷蛋白1）与lncRNA（lncRNA（结直肠癌相关1））有结合靶点。
oxLDL可上调HCAECs中lncRNA（结直肠癌相关1）的表达，进而影响细胞内lncRNA（分泌型磷蛋白1）途径调节细胞内氧化应激水平。这进而影响细胞凋亡水平和伤口愈合能力，导致细胞产生持续的炎症反应。
