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Silencing of Long Non-coding RNA H19 Alleviates Lipopolysaccharide (LPS)-induced Apoptosis and Inflammation Injury by Regulating miR-140-5p/TLR4 Axis in Cell Models of Pneumonia

[ Vol. 23 , Issue. 3 ]


Hong Yang*   Pages 275 - 284 ( 10 )


<p>Objective: Mounting studies have clarified the link between long non-coding RNAs (lncRNAs) and pneumonia. This research aims to probe the function and regulatory mechanism of lncRNA H19 in lipopolysaccharide (LPS)-induced cell models of pneumonia. <p> Methods: WI-38 cells were exposed to LPS for 12 h to mimic cell models of pneumonia. The relative expression of H19, miR-140-5p, and toll-like receptor 4 (TLR4) were detected by quantitative real-time polymerase chain reaction (qRT-PCR). The cell viability was detected by MTT assay. The protein expression of apoptosis-associated proteins (Bax and Bcl-2) and TLR4 were determined by western blot. Moreover, the content of interleukin (IL)-6, IL-1&#946;, and tumor necrosis factor (TNF)-&#945; were measured by enzyme-linked immunosorbent assay (ELISA). The target relationship between miR- 140-5p and H19/ TLR4 was confirmed by Dual luciferase reporter (DLR) assay. <p> Results: LncRNA H19 and TLR4 were up-regulated, while miR-140-5p was downregulated in peripheral blood of patients with pneumonia and LPS-treated WI-38 cells compared with their controls. Silencing of H19 or miR-140-5p mimics facilitated cell viability, whereas repressed apoptosis and reduced content of TNF-&#945;, IL-6, and IL-1&#946; in LPS-induced WI-38 cells. H19 targeted miR-140-5p and it inversely regulated miR-140- 5p expression. MiR-140-5p targeted TLR4 and it inversely regulated TLR4 expression. H19 positively regulated TLR4 expression. Moreover, inhibition of miR-140-5p or overexpression of TLR4 reversed the effects of H19 silencing on cell viability, inflammation, and apoptosis in LPS-induced WI-38 cells. <p> Conclusion: Silencing of H19 inhibited apoptosis and inflammation by miR-140- 5p/TLR4 pathway in LPS-induced WI-38 cells.</p>


Pneumonia, H19, miR-140-5p, TLR4, inflammation, apoptosis.


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