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Altered lncRNAs transcriptomic profiles in atherosclerosis-induced ischemic stroke

ABSTRACT: Long non-coding RNAs (lncRNAs) can not only regulate gene transcription and translation, but also participate in the development of central nervous system diseases as epigenetic modification factors. However, their functional significance in atherosclerosis-induced ischemic stroke (AIIS) is unclear. The study aimed to screen out differentially expressed lncRNAs (delncRNAs), and to elucidate their potential regulatory mechanisms in the pathophysiology of AIIS. We screened out 10 patients with AIIS and recruited 10 healthy volunteers. We used microarray to detect the whole blood RNA of subjects, and explored the biological functions of delncRNAs by GO and KEGG analysis. After further analyzing the delncRNAs of THP-1 stimulated by ox-LDL, selective lncRNAs were screened. Through co-expression analysis, a corresponding lncRNA-mRNA interaction network was constructed. We yielded 180 delncRNAs (44 up-regulated and 136 down-regulated) and 218 demRNAs (45 up-regulated and 173 down-regulated). Lnc-SCARNA8 and lnc-SNRPN-2 are the highest elevated and decreased lncRNA in AIIS, respectively. The delncRNAs may play a significant role in ubiquitination-mediated protein degradation signaling pathways. In THP-1 cells models, the expression levels of lnc-SLC22A16-3, lnc-MTRNR2L1-10 and lnc-ACAT1-4 were consistent to the microarray results. According to lncRNA-mRNA network, the expression of vacuolar protein sorting 13 homolog B (VPS13B) and biliverdin reductase B (BLVRB) were significantly regulated. This study identified selective delncRNAs through microarray detection and validated by in vitro cell experiment. Our findings suggest that the ubiquitinated proteasome pathway, VPS13B and BLVRB may play a fundamental role in the pathological process of AIIS.

ORGANISM(S): Homo sapiens

PROVIDER: GSE146882 | GEO | 2020/03/13

REPOSITORIES: GEO

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Project description:Adiponectin (APN) is an endogenous adipokine secreted from adipocytes that exerts an anti-inflammation property. AdipoAI is an orally active adiponectin receptor agonist identified by our group, which can emulate APN's anti-inflammatory properties through mechanisms not fully understood. To explore AdipoAI function, we used lncRNA microarray and got differential lncRNA/mRNA expression medicated by AdipoAI. Identified as one kind of non-coding RNA with more than 200bp length, lncRNA has been demonstrated to have abundance biological functions, including anti-inflammatory response. In the current study, we performed an lncRNA microarray in LPS-induced Raw264.7 cells which pre-stimulated with AdipoAI, and screened 110 DElncRNAs and 190 DEmRNAs. Enrichment analyses were conducted to total mRNAs and DEmRNAs, including GSVA, ssGSEA, GO/KEGG, GSEA and PPI analysis. Among all these processes, endocytosis was significantly enriched. A co-expression analysis was built based on DElncRNAs and DEmRNAs. Then, using Targetscan and miRwalk to predict related microRNAs of DElncRNAs and DEmRNAs respectively, we established competing endogenous RNA (ceRNA) networks including 54 mRNAs from 8 GO items. Furthermore, 33 m6A methylation related marker genes were obtained from previous study and used for the construction of m6A related-lncRNA network using the co-expression analysis. We identified FTO as the hub gene of the network, and 14 lncRNAs that interacted with it. The expression levels of 10 lncRNAs selected from ceRNA and FTO- related lncRNAs networks were validated with qRT-PCR. Finally, Macrophage phenotype scores showed that AdipoAI could attenuate the M2b and M2c polarization of macrophage and correlate with the above lncRNAs. Our work reveals that lncRNA might involve in the anti-inflammation process of AdipoAI in LPS-induced macrophages through ceRNA network and epigenetic regulation of m6A. Mechanistically, these lncRNAs associated with AdipoAI might be related to endocytosis and polarization in macrophage, and provide new candidates for the anti-inflammatory application of APN and its receptor agonist.

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Altered lncRNAs transcriptomic profiles in atherosclerosis-induced ischemic stroke

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