Chronic obstructive pulmonary disease (COPD) is an inflammatory respiratory disease. Long non-coding RNAs (lncRNAs) have been implicated in the pathogenesis of COPD. In the present study, we set to investigate the role and mechanism of LOC729178 on cigarette smoke extract (CSE)-induced inflammatory damage in 16HBE cells. The expression levels of LOC729178, miR-144-3p, and PH domain leucine-rich repeat protein phosphatase 2 (PHLPP2) were detected by quantitative real-time polymerase chain reaction (qRT-PCR) and western blot. Cell viability and apoptosis were assessed by Cell Counting Kit-8 (CCK-8) and flow cytometry, respectively. Enzyme-linked immunosorbent assay (ELISA) assay was performed to evaluate the levels of interleukin-1β (IL-1β), IL-6, tumor necrosis factor-alpha (TNF-α), and IL-8. Targeted relationships among LOC729178, miR-144-3p, and PHLPP2 were verified by dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Our data indicated that LOC729178 was underexpressed in COPD tissues and CSE-treated 16HBE cells. Exogenous expression of LOC729178 alleviated CSE-induced inflammatory injury in 16HBE cells. LOC729178 targeted miR-144-3p by directly binding to miR-144-3p. miR-144-3p was a downstream effector of LOC729178 function. PHLPP2 was identified as a direct and functional target of miR-144-3p. Furthermore, LOC729178 operated as a post-transcriptional regulator of PHLPP2 expression through miR-144-3p. Our current study suggested that LOC729178 overexpression alleviated CSE-induced inflammatory injury in 16HBE cells at least in part by up-regulating PHLPP2 via sponging miR-144-3p, providing a rationale for developing LOC729178 as a potential therapeutic agent against COPD.

慢性阻塞性肺疾病 (COPD) 是一种炎症性呼吸系统疾病。长链非编码 RNA (lncRNA) 与 COPD 的发病机制有关。在本研究中，我们着手研究 LOC729178 在香烟烟雾提取物 (CSE) 诱导的 16HBE 细胞炎症损伤中的作用和机制。通过定量实时聚合酶链反应 (qRT-PCR) 和蛋白质印迹检测 LOC729178、miR-144-3p 和 PH 结构域富含亮氨酸重复蛋白磷酸酶 2 (PHLPP2) 的表达水平。分别通过细胞计数试剂盒-8 (CCK-8) 和流式细胞术评估细胞活力和细胞凋亡。进行酶联免疫吸附测定 (ELISA) 测定以评估白细胞介素-1β (IL-1β)、IL-6、肿瘤坏死因子-α (TNF-α) 和 IL-8 的水平。LOC729178、miR-144-3p、和 PHLPP2 通过双荧光素酶报告基因和 RNA 免疫沉淀 (RIP) 测定进行验证。我们的数据表明 LOC729178 在 COPD 组织和 CSE 处理的 16HBE 细胞中表达不足。LOC729178 的外源表达减轻了 CSE 诱导的 16HBE 细胞炎症损伤。LOC729178 通过直接结合 miR-144-3p 靶向 miR-144-3p。miR-144-3p 是 LOC729178 功能的下游效应子。PHLPP2 被确定为 miR-144-3p 的直接和功能靶点。此外，LOC729178 通过 miR-144-3p 作为 PHLPP2 表达的转录后调节因子起作用。我们目前的研究表明，LOC729178 过表达至少部分是通过通过海绵 miR-144-3p 上调 PHLPP2 来减轻 CSE 诱导的 16HBE 细胞炎症损伤，