Profiling neuron-autonomous lncRNA changes upon ischemia/reperfusion injury.

Abstract

Extensive changes of neuronal transcriptome occur post ischemic stroke and during the following reperfusion. Although numerous studies focused on transcriptome changes of mRNAs associated with ischemic stroke, little is known about whether and how long non-coding RNAs (lncRNAs), which play critical roles in cellular homeostasis, are involved in this process. In this study, we performed high throughput screening to analyze expression changes of lncRNAs in primarily cultured hippocampal neurons under an oxygen-glucose deprivation/reperfusion (OGD/R) condition at 0 h, 6 h, 12 h, and 18 h, respectively. Knock down of one validated lncRNAs (Tnxa-ps1) promoted neuronal survival by inhibiting apoptosis. Coding non-coding co-expression network analysis revealed that the expression of Tnxa-ps1 was highly correlated with changes of a particular group of genes, many of which are associated with neural protection. Finally, we showed that down-regulation of Tnxa-ps1 reversed the expression changes of four mRNAs post OGD/R, revealing a regulatory effect between Tnxa-ps1 and selected genes. Together, our data revealed possible participation of lncRNAs in the pathophysiology of OGD/R and thereby provided new insights into the studies of potential therapeutic targets for ischemic stroke.

• Authors: Haiying Li, Youjia Wu, Guihai Suo, Feifei Shen, Yuqin Zhen, Xia Chen, Haitao Lv
• Journal: Biochemical and biophysical research communications (Biochem Biophys Res Commun) Vol. 495 Issue 1 Pg. 104-109 (01 01 2018) ISSN: 1090-2104 [Electronic] United States
• PMID: 29101036 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
• Copyright: Copyright © 2017 Elsevier Inc. All rights reserved.

Chemical References

• RNA, Long Noncoding
• RNA, Messenger
• RNA, Small Interfering
• Tenascin
• long non-coding RNA Tnxa-ps1, rat

Topics

• Animals
• Apoptosis
• Cell Survival
• Cells, Cultured
• Gene Expression Profiling
• Gene Knockdown Techniques
• Hippocampus (metabolism, pathology)
• Neurons (metabolism, pathology)
• RNA, Long Noncoding (antagonists & inhibitors, genetics, metabolism)
• RNA, Messenger (genetics, metabolism)
• RNA, Small Interfering (genetics)
• Rats
• Reperfusion Injury (genetics, metabolism, pathology)
• Tenascin (antagonists & inhibitors, genetics, metabolism)