Abstract
Long non-coding RNA Small Nucleolar RNA Host Gene 16 (SNHG16) has been reported to participate in Lipopolysaccharide (LPS)-induced inflammatory pathway, which contributes to pneumonia. This study was therefore conducted to explore the role of SNHG16 in pneumonia. In this study, expression of SNHG16 and microRNA (miR)-210 in pneumonia plasma samples (n = 56) and control samples (n = 60) was detected by RT-qPCR. The potential crosstalk between SNHG16 and miR-210 was analyzed by performing overexpression experiments. MSP was performed to study the role of SNHG16 in methylation of miR-210 gene. Cell apoptosis was analyzed by cell apoptosis assay. Decreased expression levels of SNHG16 and increased expression levels of miR-210 were observed in pneumonia. SNHG16 showed an inverse correlation to miR-210. LPS treatment led to downregulated SNHG16 and upregulated miR-210 in Human Bronchial Epithelial Cells (HBEpCs). In HBEpCs, SNHG16 downregulated miR-210 and increased miR-210 DNA gene methylation. Moreover, SNHG16 suppressed the role of miR-210 in cell apoptosis under LPS treatment. In conclusion, SNHG16 is downregulated in pneumonia, and it downregulates miR-210 possibly through methylation to promote lung cell apoptosis induced by LPS.
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Supplementary file1 The role of overexpression of SNHG16 and miR-210 in regulating the expression of SNHG16 and miR-210 in medium. Culture medium of HBEpCs was collected at 48-h post-transfection to detect circulating miR-210 (A) and SNHG16 (B). *, p < 0.05 (TIF 92 KB)
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Gao, P., Wang, J., Jiang, M. et al. LncRNA SNHG16 is Downregulated in Pneumonia and Downregulates miR-210 to Promote LPS-Induced Lung Cell Apoptosis. Mol Biotechnol 65, 446–452 (2023). https://doi.org/10.1007/s12033-022-00545-6
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DOI: https://doi.org/10.1007/s12033-022-00545-6