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LncRNA SNHG14 promoted inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis

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Abstract

Background

Cerebral apoplexy is currently the main cause of mortality and disability globally. LncRNAs play important roles in the pathophysiological process of cerebral apoplexy and the effect of LncRNA SNHG14 on cerebral apoplexy remain unclear.

Objective

Here, we investigated the biological function of LncRNA SNHG14 in cerebral apoplexy and underlying molecular mechanisms.

Results

Patients with cerebral apoplexy and normal volunteers were collected. Mouse hippocampal (HT-22) cells were then placed into a hypoxic incubator with 1% O2, 5% CO2, and 94% N2 for cerebral apoplexy. LncRNA SNHG14 was overexpressed in patients with cerebral apoplexy. LncRNA SNHG14 was found to induce inflammation in vitro model of cerebral apoplexy via the inhibition of miR-124-3p/TRAF6 axis. In addition, the down-regulation of LncRNA SNHG14 reduced inflammation in vitro model of cerebral apoplexy via the induction of miR-124-3p/TRAF6 axis.

Conclusion

LncRNA SNHG14 plays a crucial role in inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis, thereby it may be a promising therapeutic target for cerebral apoplexy.

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Acknowledgements

This work was supported by The First Affiliated Hospital of Harbin Medical University Research Fund (No. 2014B24).

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FL contributed to data analysis, drafting or revising the article, gave final approval of the version to be published, and agreed to be accountable for all aspects of the work.

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Correspondence to Fang Li.

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Fang Li declares that she has no conflict of interest.

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All the samples were obtained following patients’ written consent and approval by the Ethics Committee of The First Affiliated Hospital of Harbin Medical University.

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Li, F. LncRNA SNHG14 promoted inflammation of cerebral apoplexy by miR-124-3p/TRAF6 axis. Mol. Cell. Toxicol. 18, 233–241 (2022). https://doi.org/10.1007/s13273-021-00197-8

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