Abstract
Functioning as miRNA sponges, long non-coding RNA (lncRNA) exert its pharmacological action via regulating expression of protein-coding genes. However, the lncRNA-mediated ceRNA in cerebral Infarction (CI) remains unclear. In this study, the expression recordsets of mRNA, lncRNA and miRNA of CI samples were obtained from the NCBI GEO datasets separately. The differentially expressed lncRNAs (DELs), miRNAs (DEMis) and mRNAs (DEMs) were identified by limma package in R platform. A total of 267 DELs, 26 DEMis, and 760 DEMs were identified as differentially expressed profiles, with which we constructed the ceRNA network composed of DELs-DEMis-DEMs. Further, clusterProfiler package in R platform is employed for performing Gene Ontology (GO) and KEGG pathway analysis. An aberrant ceRNA network was constructed according to node degrees in CI, including 28 DELs, 19 DEMs and 12 DEMis, from which we extracted the core network, in which 9 nodes were recognized as kernel genes including Tspan3, Eif4a2, rno-miR-208a-3p, rno-miR-194-5p, Pdpn, H3f3b, Stat3, Cd63 and Sdc4. Finally, with the DELs-DEMis-DEMs ceRNA network provided above, we can improve our understanding of the pathogenesis of CI mediated by lncRNA.
Highlights
Stroke is a very high risk factor for death and/or disability in the world,80% of which would be blamed for cerebral ischemic due to thromboembolic occlusion in the cerebral artery[1,2]
More and more attention has been put into the regulatory network composed of long non-coding RNAs, microRNAs and messenger RNAs to clarify the mechanisms underlying in cerebral Infarction (CI)
The expression levels of long non-coding RNA (lncRNA) in 5 middle cerebral artery occlusion (MCAO) operated rats and 5 Sham operated rats were investigated in this study
Summary
Stroke is a very high risk factor for death and/or disability in the world,80% of which would be blamed for cerebral ischemic due to thromboembolic occlusion in the cerebral artery[1,2]. Necropsy analyses of patients died of stroke indicate a high prevalence of coronary atherosclerosis and myocardial infarction[6,7]. It is still vague what the behind molecular progressions of CI are. Yan et al.[13] uncovered the MEG3/ miR-21/PDCD4 ceRNA strategy as a novel therapeutic intervention in regulating the molecular mechanisms of cerebral ischemic stroke. Chen et al.[14] indicated that GAS5 acted as a ceRNA for miR-137/Notch[1] signaling pathway to promote the progression of ischemic stroke form which an extensive understanding and novel therapeutic options for CI are provided
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