Retracted: Protective impacts of long noncoding RNA taurine‐upregulated 1 against lipopolysaccharide‐evoked injury in MRC‐5 cells through inhibition of microRNA‐127

Abstract

Background Pneumonia is a respiratory disease, which is triggered by pathogenic microorganisms or physical/chemical factors. Increasing evidence confirmed the vital impacts of long noncoding RNAs on various inflammatory diseases. Nonetheless, the influence of taurine‐upregulated 1 (TUG1) in pneumonia remains vague. The research tried to disclose the protective impacts of TUG1 against lipopolysaccharide (LPS)‐evoked injury in MRC‐5 cells. Methods MRC‐5 cells were disposed with LPS to construct pulmonary injury model. Then, pc‐TUG1 vector was transfected into MRC‐5 cells and the influence of overexpressed TUG1 in cell viability, apoptosis, and pro‐inflammatory cytokines in LPS‐disposed cells were evaluated. The correlation between TUG1 and microRNA (miR)−127 was estimated via utilizing real‐time quantitative polymerase chain reaction (RT‐qPCR), meanwhile whether miR‐127 affected the impacts of TUG1 on LPS‐injured MRC‐5 cells was explored. Besides, NF‐κB and p38MAPK pathways were evaluated to understand the dormant mechanisms. Results LPS administration apparently evoked inflammatory injury in MRC‐5 cells by restraining cell viability, accelerating apoptosis, and enhancing TNF‐α and IL‐6 productions. But, TUG1 lightened LPS‐evoked pro‐inflammatory response in MRC‐5 cells. In addition, miR‐127 was repressed by overexpressed TUG1, meanwhile the protective impacts of TUG1 against LPS‐evoked inflammatory injury in MRC‐5 cells were overturned by overexpressed miR‐127. Finally, we disclosed that TUG1 hindered the activation of NF‐κB and p38MAPK pathways via restraining miR‐127. Conclusions These explorations testified that taurine‐upregulated 1 (TUG1) protected MRC‐5 cells against lipopolysaccharide (LPS)‐evoked inflammatory injury via hindering miR‐127/NF‐κB/p38MAPK axis.

Long Non-coding RNA TUG1 Modulates Expression of Elastin to Relieve Bronchopulmonary Dysplasia via Sponging miR-29a-3p

“…Qiu et al have revealed that TUG1 shows a protective effect on LPS-induced primary murine pulmonary microvascular endothelial cells and ameliorates sepsis-induced inflammation and pulmonary injury in mice (29). Moreover, TUG1 is reported to alleviate LPS-evoked inflammatory response in pneumonia (14). Similar to the results of the above literature, we also found that overexpression of TUG1 alleviated inflammation and pulmonary injury of BPD mice.…”

“…Because miR-29a-3p and miR-29b are different isoforms of the miR-29 family, they may exert different functions in BPD. Increasing studies have demonstrated that TUG1 is involved in the progression of pulmonary injury and hypoxic pulmonary hypertension (HPH) via sponging miR-127 (14) and miR-374c (36). In the current study, we found that miR-29a-3p acted as a downstream target of TUG1 in hyperoxiainduced MLE-12 cells, which was inversely regulated with TUG1.…”

“…Notably, lncRNA taurine upregulated gene 1 (TUG1) with 6.7 kb nucleotides is located at chromosome 22q12 (12). Growing literature has indicated that dysregulation of TUG1 is involved in lung-related diseases, such as chronic obstructive pulmonary disease (COPD) (13), pneumonia (14), and pulmonary arterial hypertension (PAH) (15). Nonetheless, there is no evidence clarifying the role of TUG1 in BPD.…”

Retracted: Emodin relieved lipopolysaccharide‐evoked inflammatory damage in WI‐38 cells by up‐regulating taurine up‐regulated gene 1

“…24 Meanwhile, other research displayed that TUG1 exerted its efficacies in pneumonia through NF-κB and p38MAPK signal pathways. 17 In this article, we put forward that emodin could significantly restrain NF-κB and p38MAPK pathways. Besides, results verified that when SB203580 and BAY11-7082 were, respectively, appended in TUG1 silenced cells, the expressions of IL-6 and MCP-1were conspicuously declined.…”

Non-coding RNAs in pneumonia diagnosis

“…В то же время сверхэкспрессия miR-127 подавляла антиапоптотическое действие TUG1. Показано, что протективное действие TUG1 в ходе воспалительной реакции обусловлено регуляцией сигнальных путей NF-κB/p38MAPK [57].…”