Long non-coding RNA TUG1 alleviates LPS-induced injury of PC-12 cells by down-regulating microRNA-127

The limited therapeutic strategies and the unsatisfied prognosis for spinal cord injury (SCI) make the identification of innovative therapeutic targets for SCI become very urgent. Herein, we explored the role of long non-cording RNA taurine up-regulated gene 1 (lncRNA TUG1) in lipopolysaccharide (LP...

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Veröffentlicht in:Experimental and molecular pathology 2019-10, Vol.110, p.104287
Hauptverfasser: Zheng, Huajiang, Hu, Shanshan, Cao, Jin, Yao, Lufeng, Zhang, Nan
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Sprache:eng
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Zusammenfassung:The limited therapeutic strategies and the unsatisfied prognosis for spinal cord injury (SCI) make the identification of innovative therapeutic targets for SCI become very urgent. Herein, we explored the role of long non-cording RNA taurine up-regulated gene 1 (lncRNA TUG1) in lipopolysaccharide (LPS)-treated PC-12 cells and studied the downstream effector and signaling cascades. We found that LPS-induced decrease of cell viability, increase of apoptosis and release of IL-6 and TNF-α were mitigated by TUG1 overexpression. MicroRNA (miR-127) was negatively regulated by TUG1. Effects of TUG1 on LPS-treated PC-12 cells were reversed by miR-127 overexpression. Besides, TUG1 inactivated NF-κB and p38MAPK pathways in LPS-treated PC-12 cells via down-regulating miR-127. Dynactin 4 and protein tyrosine phosphatase (PTP) were the target genes of miR-127. miR-127 regulated the NF-κB and p38MAPK pathways in PC-12 cells at least by targeting dynactin 4 and PTP. In conclusion, we discovered that TUG1 alleviated LPS-induced PC-12 cell inflammatory injury might be through down-regulating miR-127, influencing dynactin 4 and PTP, and then inactivating NF-κB and p38MAPK pathways.
ISSN:1096-0945
DOI:10.1016/j.yexmp.2019.104287