ANRIL siRNA Microarray Data in HUVECs
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ABSTRACT:
PROVIDER: PRJNA482871 | ENA |
REPOSITORIES: ENA
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Project description:Long non-coding RNAs（LncRNAs）have important cellular functions and some have roles in different mechanisms of gene regulation. LncRNA-antisense noncoding RNA in the INK4 locus (ANRIL) were found to affect cell inflammation,Nevertheless, the potential genes related to the inflammatory response regulated by ANRIL remain unclear. In this study, we investigated the potential function of ANRIL in regulating expression and alternative splicing. ANRIL-regulated human umbilical vein endothelial (HUVEC) cell transcriptome achieved by high-throughput RNA sequencing(RNA-seq) was obtained to investigate the potential role of ANRIL. Lipofectamine 2000 was used for plasmid transfection. The gene expression profile and alternative splicing pattern of HUVEC overexpressed by ANRIL were analyzed by RNA-seq and compared with the control group. ANRIL overexpression (ANRIL-OE) widely affects the transcription levels of genes related to inflammatory response, NF-κB pathway, type I interferon-mediated signal transduction pathway, and innate immune response. ANRIL extensively regulates the alternative splicing of hundreds of genes through functions such as gene expression, translation, DNA repair, RNA processing, and NF-κB pathway. Many of these genes have an indispensable role in the inflammatory response. ANRIL regulated inflammatory response may be achieved by regulating alternating splicing and potential transcription, which broadens the understanding of ANRIL-mediated gene regulation mechanisms and clarifies the role of ANRIL in mediating inflammatory response mechanisms.
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2014-09-25 | E-GEOD-41180 | biostudies-arrayexpress
Project description:To examine the role of WTAP in splicing regulation, we performed high-throughput mRNA sequencing (RNA-seq) on RNA isolated from control, WTAP or Virilizer siRNA-treated HUVECs, yielding 12 million uniquely mapped 75nt pair-end tags from each sample. MapSplice software was used for differential expression and differences in transcript splice junctions .
2014-09-25 | GSE41180 | GEO
Project description:KLF2 and KLF4 are important transcriptional factors in endothelial cells, however their roles in statin treatment has not been elucidated. Here we report the comprehensive change of transcripts of statin treated HUVECs transfected with siRNA KLF2 or KLF4. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4hours. Before statin treatment, cells were transfected with siRNA KLF2 or KLF4.
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Project description:To determine the role of HBO1 in EC physiology, gene expression analysis was conducted on control and HBO1 siRNA-treated HUVECs. A total of 263 differentially regulated protein-coding transcripts were detected, many of which are key for growth and angiogenesis. Additionally, many genes involved in cell cycle, cell division, and DNA replication were dysregulated. HBO1-regulated genes were verified by qRT-PCR, including those with roles in vessel tone regulation (e.g. ACE1), vessel formation (e.g. CXCL16), EC activation (e.g. E-selectin), and cholesterol efflux (e.g. ABCG1).
2018-01-19 | GSE93608 | GEO
Project description:KLF2 and KLF4 are important transcriptional factors in endothelial cells, however their roles in statin treatment has not been elucidated. Here we report the comprehensive change of transcripts of statin treated HUVECs transfected with siRNA KLF2 or KLF4. We used repeated microarray analysis of HUVECs treated with pitavastatin for 4hours. Before statin treatment, cells were transfected with siRNA KLF2 or KLF4. HUVECs were used within the first 6 passages. For studies, HUVECs were cultivated in medium EGM2MV containing pitavastatin at a concentration of 1 micromolar.
2013-01-01 | E-GEOD-32693 | biostudies-arrayexpress
Project description:The antisense non-coding RNA in the INK locus (ANRIL), which originates from the CDKN2A/B (INK4-ARF) locus, has been identified as a hotspot for genetic variants associated with cardiometabolic disease including coronary artery disease (CAD) and Type 2 diabetes (T2D). We recently found that ANRIL abundance in human pancreatic islets was increased in donors carrying certain T2D risk-SNPs, and that a T2D risk-SNP located within exon2 of ANRIL conferred reduced beta cell proliferation index, pointing to a role for ANRIL in the regulation of T2D pathogenicity via an impact on insulin secretory capacity. Recent studies in other cell types have found that the balance between linear and circular species of ANRIL is linked to the regulation of cardiovascular disease phenotypes. Less is known about circular ANRIL expression in diabetes-relevant cell types and how their abundance might influence the risk of T2D. Herein, we use high-throughput and divergent primer sequencing of circular RNA in human pancreatic islet cells to quantify and characterize circular isoforms of ANRIL. We identified several circular ANRIL isoforms that are more abundant than linear ANRIL and whose expression was correlated across dozens of individuals. Back-splicing did not occur with equal probability at all ANRIL splice sites. Rather, some specific splice sites were found to have a higher propensity to be involved in back-splicing and are weakly enriched for sequence features known to promote back-splicing. Finally, we found that islets from carriers of the T2D risk allele at rs564398 in exon 2 of ANRIL had a higher ratio of circular ANRIL relative to linear ANRIL compared to protective-allele carriers, and that higher circular:linear ANRIL ratio was associated with a decreased beta cell proliferation index. Together, our study points to the combined involvement of both linear and circular ANRIL species in T2D phenotypes and opens the door for future studies to understand the molecular mechanisms by which ANRIL impacts cellular function in human pancreatic islets.
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Project description:Expression data from Ang II induced HUVECs
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Project description:lncRNAs were associated with the cardiovascular diseases since we used Affy lncRNA gene expression microarray to analyze differentially expressed lncRNAs in both normal and Ang II induced HUVECs
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