Department of Emergency, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Department of Critical Care Medicine, The Affiliated Changzhou No.2 People's Hospital of Nanjing Medical University, Changzhou, Jiangsu, China.
Bioengineered. 2022 May;13(5):13643-13653. doi: 10.1080/21655979.2022.2083820.
Airway inflammation is associated with various respiratory diseases, and previous research has confirmed that long non-coding RNAs (lncRNAs) play imperative roles in inflammatory responses. However, the function of lncRNA SOX2 overlapping transcript (SOX2-OT) in airway inflammation remains enigmatic. This study aimed to investigate the effects of SOX2-OT on lipopolysaccharide (LPS)-induced cell injury in human bronchial epithelial cells, BEAS-2B, and its potential mechanisms. The results showed increased cell apoptotic ratio, production of inflammatory cytokines, higher expression of adhesion molecules and activation of NF-κB in LPS-stimulated BEAS-2B cells. In LPS-stimulated BEAS-2B cells, SOX2-OT up-regulation and miR-455-3p down-regulation emerged simultaneously. SOX2-OT knockdown or miR-455-3p over-expression restrained LPS-induced inflammation and injury. SOX2-OT sponged to miR-455-3p and functioned as a ceRNA. In addition, phosphatase and tensin homolog (PTEN) served as an endogenous target of miR-455-3p to modulate the phosphatidylinositol 3-kinase/protein kinase B (PI3K/AKT) pathway and disturb the alleviated consequence of miR-455-3p over-expression on LPS-induced BEAS-2B cell inflammation and cell injury. Our data demonstrated that SOX2-OT plays a pivotal role in LPS-induced inflammation and injury in BEAS-2B cells and exerts its function through the miR-455-3p/PTEN axis and modulation of the PI3K/AKT pathway.
气道炎症与各种呼吸道疾病有关，先前的研究已经证实长链非编码 RNA（lncRNA）在炎症反应中发挥着重要作用。然而，lncRNA SOX2 重叠转录物（SOX2-OT）在气道炎症中的功能仍然是个谜。本研究旨在探讨 SOX2-OT 对人支气管上皮细胞（BEAS-2B）中脂多糖（LPS）诱导的细胞损伤的影响及其潜在机制。结果表明，LPS 刺激的 BEAS-2B 细胞中细胞凋亡比例增加，炎症细胞因子产生增加，黏附分子表达上调，NF-κB 激活。在 LPS 刺激的 BEAS-2B 细胞中，SOX2-OT 上调和 miR-455-3p 下调同时出现。SOX2-OT 敲低或 miR-455-3p 过表达抑制了 LPS 诱导的炎症和损伤。SOX2-OT 可与 miR-455-3p 结合并作为 ceRNA 发挥作用。此外，磷酸酶和张力蛋白同源物（PTEN）作为 miR-455-3p 的内源性靶标，调节磷脂酰肌醇 3-激酶/蛋白激酶 B（PI3K/AKT）通路，并干扰 miR-455-3p 过表达对 LPS 诱导的 BEAS-2B 细胞炎症和细胞损伤的缓解作用。我们的数据表明，SOX2-OT 在 LPS 诱导的 BEAS-2B 细胞炎症和损伤中发挥着关键作用，通过 miR-455-3p/PTEN 轴和 PI3K/AKT 通路的调节来发挥其功能。
