Atherosclerosis (AS) is the typical cardiovascular disease, which is the main underlying inducement of cardiovascular diseases. Aberrant expression of long noncoding RNA HLA complex group 11 (HCG11) was engaged with atherosclerosis. The objective of the present research was to explore the role and the potential mechanism of HCG11 in AS. Human umbilical vein endothelial cells (HUVECs) were stimulated with oxidized low-density lipoprotein (ox-LDL) to induce the AS model in vitro. The cell viability was detected by MTT assay. Flow cytometry was performed to determine cell pyroptosis. Gene and protein levels were detected by qPCR or Western blot assay. The interaction between HCG11, miR-224-3p, and Janus kinase 1 (JAK1) was validated by dual-luciferase reporter assays. Ox-LDL treatment aggravated cell pyroptosis and inflammation in HUVECs. And the levels of HCG11 and JAK1 was enhanced in ox-LDL-induced HUVECs, while miR-224-3p expression was reduced. Additionally, knockdown of HCG11 or miR-224-3p overexpression reversed the ox-LDL-induced cell viability decline and the increase of cell pyroptosis and inflammation-related proteins, including gasdermin D N-terminal (GSDMD-N), Caspase-1, NOD-like receptor family pyrin domain-containing 3 (NLRP3), interleukin 18 (IL-18), and interleukin 1beta (IL-1β). Moreover, HCG11 could modulate the JAK1 expression via targeting miR-224-3p. The inhibitory effect of HCG11 silencing on cell pyroptosis and inflammation was reversed by miR-224-3p knockdown. Furthermore, overexpression of miR-224-3p could repress the ox-LDL-induced cell pyroptosis and inflammation via regulating JAK1 expression. Knockdown of HCG11 alleviated cell pyroptosis and inflammation induced by ox-LDL via targeting the miR-224-3p/JAK1 axis, indicating that HCG11 could be the latent target of diagnosis or treatment for AS.

动脉粥样硬化(AS)是典型的心血管疾病，是心血管疾病的主要潜在诱因。长链非编码 RNA HLA 复合物组 11 (HCG11) 的异常表达与动脉粥样硬化有关。本研究的目的是探讨 HCG11 在 AS 中的作用和潜在机制。用氧化低密度脂蛋白 (ox-LDL) 刺激人脐静脉内皮细胞 (HUVEC) 以在体外诱导 AS 模型。MTT法检测细胞活力。进行流式细胞术以确定细胞焦亡。通过 qPCR 或蛋白质印迹分析检测基因和蛋白质水平。HCG11、miR-224-3p 和 Janus 激酶 1 (JAK1) 之间的相互作用通过双荧光素酶报告基因检测得到验证。Ox-LDL 治疗加重了 HUVEC 中的细胞焦亡和炎症。并且 ox-LDL 诱导的 HUVEC 中 HCG11 和 JAK1 的水平增强，而 miR-224-3p 表达降低。此外，敲低 HCG11 或 miR-224-3p 过表达可逆转 ox-LDL 诱导的细胞活力下降以及细胞焦亡和炎症相关蛋白的增加，包括 gasdermin D N-末端 (GSDMD-N)、Caspase-1、 NOD 样受体家族含有 pyrin 结构域 3 (NLRP3)、白细胞介素 18 (IL-18) 和白细胞介素 1beta (IL-1β)。此外，HCG11 可以通过靶向 miR-224-3p 来调节 JAK1 的表达。HCG11 沉默对细胞焦亡和炎症的抑制作用被 miR-224-3p 敲低逆转。此外，miR-224-3p 的过表达可以通过调节 JAK1 表达来抑制 ox-LDL 诱导的细胞焦亡和炎症。