长链非编码 RNA GAS5 通过下调 miR-155 抑制细胞凋亡并促进 SHIP-1 表达参与儿童肺炎的发生。
LncRNA GAS5 participates in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.
机构信息
Department of Respiratory and Critical Medicine, Clinical Medical College of Hulunbeier, Inner Mongolia University for Nationalities, Hulunbuir People's Hospital, Hulunbuir City, 021008, Inner Mongolia, People's Republic of China.
出版信息
BMC Pulm Med. 2021 Nov 11;21(1):362. doi: 10.1186/s12890-021-01724-y.
BACKGROUND
LncRNA GAS5 and miR-155 are reported to play opposite roles in lung inflammatory responses. Lung inflammation participates in childhood pneumonia, indicating the involvement of GAS5 and miR-155 in pneumonia. The study aimed to analyze the potential interaction between GAS5 and miR-155 in childhood pneumonia.
METHODS
GAS5 and miR-155 levels in plasma samples from pneumonia patients and controls were detected using RT-qPCR. The role of GAS5 in miR-155 RNA gene methylation in human bronchial epithelial cells (HBEpCs) was analyzed by methylation analysis. Flow cytometry and RT-qPCR were applied to analyze cell apoptosis and SHIP-1 expression, respectively.
RESULTS
GAS5 was downregulated in pneumonia, and miR-155 was upregulated in pneumonia. GAS5 and miR-155 were inversely correlated. GAS5 overexpression decreased miR-155 expression in HBEpCs, while miR-155 overexpression showed no significant effects on GAS5 expression. In addition, GAS5 suppressed LPS-induced HBEpC apoptosis, promoted SHIP-1 expression, and reduced the enhancing effect of miR-155 on cell apoptosis and SHIP-1 expression.
CONCLUSIONS
GAS5 may participate in childhood pneumonia by inhibiting cell apoptosis and promoting SHIP-1 expression via downregulating miR-155.
背景
长链非编码 RNA GAS5 和 miR-155 在肺部炎症反应中发挥相反的作用。肺部炎症参与儿童肺炎，表明 GAS5 和 miR-155 参与肺炎。本研究旨在分析 GAS5 和 miR-155 之间在儿童肺炎中的潜在相互作用。
方法
采用 RT-qPCR 检测肺炎患者和对照者血浆样本中的 GAS5 和 miR-155 水平。通过甲基化分析分析 GAS5 对人支气管上皮细胞 (HBEpC) 中 miR-155 RNA 基因甲基化的作用。采用流式细胞术和 RT-qPCR 分别分析细胞凋亡和 SHIP-1 表达。
结果
肺炎中 GAS5 下调，肺炎中 miR-155 上调。GAS5 和 miR-155 呈负相关。GAS5 过表达降低了 HBEpC 中的 miR-155 表达，而 miR-155 过表达对 GAS5 表达没有显著影响。此外，GAS5 抑制 LPS 诱导的 HBEpC 凋亡，促进 SHIP-1 表达，并降低 miR-155 对细胞凋亡和 SHIP-1 表达的增强作用。
结论
GAS5 可能通过下调 miR-155 抑制细胞凋亡和促进 SHIP-1 表达参与儿童肺炎。
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