Song Zhenhua, Han Qianqian, Wen Ziyun, Lv Qing, Pan Chao, Pan Yunyun
Treatment Centre for Traumatic Injuries, The Third Affiliated Hospital of Southern Medical University, Guangzhou, China.
The First Affiliated Hospital of Guangdong Pharmaceutical University, Guangzhou, China.
Ann Transl Med. 2023 Feb 15;11(3):143. doi: 10.21037/atm-22-6457. Epub 2023 Feb 9.
Long noncoding RNA (lncRNA)-mediated changes in gene expression contribute to atherosclerosis (AS) development. However, the roles of numerous lncRNAs in AS have not been fully elucidated. Here, we aimed to investigate the potential role of () in autophagy of human aortic vascular smooth muscle cells (HA-VSMCs).
expression in patients with AS was extracted from the Gene Expression Omnibus (GEO) database. and microRNA-188-3p () expression was analyzed in 20 enrolled patients with AS. HA-VSMCs were treated with oxidized low-density lipoprotein (ox-LDL) (25, 50, 75, and 100 µg/mL) for 24 h. Loss- or gain-of-function of , miR-1883p, and autophagy-related 7 () was studied using the transfected HA-VSMCs. Cell viability was assessed using Cell Counting Kit-8 (CCK-8). Apoptosis was detected with annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI). Relative luciferase reporter assay was used to confirm the targeting relationship of to or . Gene expression was detected by quantitative real-time reverse transcription-polymerase chain reaction (qRT-PCR) and Western blot.
was enriched in the serum of patients with AS and ox-LDL-treated HA-VSMCs. Ox-LDL induced proliferation and autophagy while inhibiting the apoptosis of HA-VSMCs, which was abated by knockdown. downregulated of ox-LDL-treated HA-VSMCs. knockdown caused an increase in , which inhibited proliferation and autophagy and induced the apoptosis of ox-LDL-treated HA-VSMCs. inhibited expression in ox-LDL-treated HA-VSMCs. elevated and induced autophagy through sponging in ox-LDL-treated HA-VSMCs.
regulated autophagy by targeting , a messenger RNA-binding miRNA that increases level, which may be a new target molecule for the prevention and prognosis of AS.
长链非编码RNA（lncRNA）介导的基因表达变化有助于动脉粥样硬化（AS）的发展。然而，众多lncRNA在AS中的作用尚未完全阐明。在此，我们旨在研究（）在人主动脉血管平滑肌细胞（HA-VSMCs）自噬中的潜在作用。
从基因表达综合数据库（GEO）中提取AS患者的（）表达。分析了20例入选的AS患者的（）和微小RNA-188-3p（）表达。用氧化低密度脂蛋白（ox-LDL）（25、50、75和100μg/mL）处理HA-VSMCs 24小时。使用转染的HA-VSMCs研究（）、miR-1883p和自噬相关7（）的功能丧失或获得。使用细胞计数试剂盒-8（CCK-8）评估细胞活力。用膜联蛋白V-异硫氰酸荧光素（FITC）和碘化丙啶（PI）检测细胞凋亡。使用相对荧光素酶报告基因测定法确认（）与（）或（）的靶向关系。通过定量实时逆转录-聚合酶链反应（qRT-PCR）和蛋白质免疫印迹法检测基因表达。
（）在AS患者血清和ox-LDL处理的HA-VSMCs中富集。ox-LDL诱导HA-VSMCs增殖和自噬，同时抑制其凋亡，（）敲低可减弱这种作用。（）下调ox-LDL处理的HA-VSMCs中的（）。（）敲低导致（）增加，抑制ox-LDL处理的HA-VSMCs的增殖和自噬并诱导其凋亡。（）抑制ox-LDL处理的HA-VSMCs中的（）表达。（）通过在ox-LDL处理的HA-VSMCs中吸附（）来升高（）并诱导自噬。
（）通过靶向（）调节自噬，（）是一种增加（）水平的信使RNA结合微小RNA，这可能是AS预防和预后的新靶分子。
