The Role of Non-Conserved Long Noncoding RNA, RP11-184M15.1, in Human Macrophage Function
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ABSTRACT:
PROVIDER: PRJNA903136 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22333187_1.fastq.gz | Fastqsanger.gz | |||
| SRR22333187_2.fastq.gz | Fastqsanger.gz | |||
| SRR22333188_1.fastq.gz | Fastqsanger.gz | |||
| SRR22333188_2.fastq.gz | Fastqsanger.gz | |||
| SRR22333189_1.fastq.gz | Fastqsanger.gz |
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Project description:Through deep RNA-seq of human monocyte-derived macrophages, we identified RP11-184M15.1, a human macrophage-specific lincRNA, to be highly induced in the cytoplasm of IL-4-stimulated macrophage. Preliminary data showed that treatment of IL-4-stimulated THP1 human macrophages with RP11-184M15.1 small interfering RNA (siRNA) repressed apoptosis of resolving macrophages, as shown by decreased Annexin V+ macrophages, and reduced protein expression of cleaved PARP. Biotinylated RP11-184M15.1 pulldown coupled with mass spectrometry indicated an interaction between RP11-184M15.1 and zinc finger RNA-binding protein (ZFR). RIP corroborated the proposed interaction between RP11-184M15.1 and ZFR. RNAInter revealed mRNAs predicted to interact with ZFR, and some of those genes (e.g., ALYREF, CCNYL1) were also differentially expressed in RNA-seq data of control versus RP11-184M15.1 knockdown in IL-4-stimulated THP1 macrophages. qPCR validated that ALYREF and CCNYL1 expression are reduced with RP11-184M15.1 knockdown. In contrast, with ZFR siRNA, ALYREF and CCNYL1 mRNA expressions were elevated. Thus, a hypothesis to be further tested is that RP11-184M15.1 interacts with ZFR to regulate mRNA stability in IL-4-stimulated macrophages. Nuclear RNA export factor 1 (NXF1) was also validated by RIP to interact with RP11-184M15.1. NXF1 is a known interacting partner of ALYREF in the transcription-export (TREX) complex. With RP11-184M15.1 knockdown, the protein level of ALYREF decreased, and Ingenuity Pathway Analysis (IPA) of RNA-seq data of control versus RP11-184M15.1 knockdown revealed that THO complex subunit 5 homolog (THOC5), another component of the TREX complex, may be an upstream regulator. In addition, past studies have revealed that ALYREF and NXF1 are involved in nuclear export of inflammatory mRNAs and proinflammatory macrophage phenotype, respectively. With RP11-184M15.1 knockdown, there was decreased expression of inflammatory macrophage-associated genes. It may be possible that RP11-184M15.1 functions in mRNA export, along with NXF1 and ALYREF.
2022-11-23 | GSE218308 | GEO
Project description:Methods and Materials The high throughput RNA sequencing (RNA-seq) data from kidney biopsies of LN patients and controls was applied studied to screen for candidate lncRNAs. Quantitative real-time polymerase chain reaction(RT-qPCR) was used to detect the expression of lncRNAs and individual IFN-stimulated genes (ISGs). Western blotting and dual-luciferace luciferase reporter assay was adopted to explore the specific function of the candidate lncRNA. Results The expression of lncRNA RP11-2B6.2 was significantly increased in the kidney tissues from LN patients compared with those from healthy controls, and positive correlated with the degree of disease activity and renal injuryinjuries. Additionally, expression of LncRNA RP11-2B6.2 could be stimulated by type I IFN. Silencing it RP11-2B6.2 significantly reduced the expression of a group of interferon-stimulating genes(ISGs) including IFIT1, OAS1, etc., Furthermore, it lncRNA RP11-2B6.2 affected the expression of IFN alpha and beta receptor subunit 1 (IFNAR1), phosphorylation of Jak1 and Stat1, and the luciferase activity induced by interferon stimulated response element(ISRE). Conclusion Long noncoding RNA RP11-2B6.2 is a positive regulator of the type I IFN signaling pathway in LN. It LncRNA RP11-2B6.2 may contribute to the pathogenesis of LN and provide served as a potentially therapeutic target.
2019-05-01 | GSE98422 | GEO
Project description:1. Evaluate the diagnostic value of long noncoding RNA (CCAT1) expression by RT-PCR in peripheral blood in colorectal cancer patients versus normal healthy control personal.
2. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in diagnosis of colorectal cancer patients & its relation to tumor staging.
3. Evaluate the clinical utility of detecting long noncoding RNA (CCAT1) expression in precancerous colorectal diseases.
4. Compare long noncoding RNA (CCAT1) expression with traditional marker; carcinoembryonic antigen (CEA) and Carbohydrate antigen 19-9 (CA19-9) in diagnosis of colorectal cancer.
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Project description:RP11-115N4.1 was identified as the most differentially expressed lncRNA which was highly upregulated in peripheral blood of non-pregnant URSA patients (P = 3.63E-07, Fold change = 2.96),andthis dysregulation was further validated in approximately 26.7% additional patients (4/15). RP11-115N4.1 expression was detected in both lymphocytes and monocytes of human peripheral blood, andin vitro overexpression of RP11-115N4.1 decreased cell proliferation in K562 cellssignificantly. Furthermore, heat-shock HSP70 genes (HSPA1A and HSPA1B) were found to be significantly upregulated upon RP11-115N4.1 overexpression by transcriptome analysis (HSPA1A (P = 4.39E-08, Fold change = 4.17), HSPA1B (P = 2.26E-06, Fold change = 2.99)).RNApull down and RNA immunoprecipitation assay (RIP) analysis demonstrated that RP11-115N4.1 bound to HNRNPH3 protein directly, which in turn activateheat-shock proteins (HSP70) analyzed by protein-protein interaction and HNRNP` knockdown assays. Most importantly,the high expression of HSP70 was also verified in the serum of URSA patients and the supernatant of K562 cells with RP11-115N4.1 activation, andHSP70 in supernatant can exacerbate inflammatory responses in monocytes by inducing IL-6, IL-1β and TNF-α and inhibit the migration of trophoblast cells, which might associate with URSA.
2021-08-11 | GSE179996 | GEO
Project description:Sepsis-induced acute lung injury (ALI) poses a significant threat to human health, necessitating further investigation into its underlying mechanisms. Long noncoding RNAs (lncRNAs) have emerged as key regulators in various diseases, including sepsis. In our prior research, we observed significant downregulation of lncRNA RP11-284N8.3 in the blood samples of sepsis patients. Herein, we elucidate the functional role and regulatory molecular targets of RP11-284N8.3 in lipopolysaccharide (LPS)-exposed BEAS-2B cells. Initially, we found that LPS treatment notably repressed RP11-284N8.3 expression. However, overexpression of RP11-284N8.3 significantly promoted cell proliferation, inhibited apoptosis, and attenuated IL-1β expression in response to LPS stimulation, indicative of its anti-inflammatory properties. Further RNA-seq analysis revealed that RP11-284N8.3 might have contributed to the significant down-regulation of genes associated with the inflammatory response, while genes related to cell cycle/division and apoptosis underwent alternative splicing (AS) deregulation. Finally, RT-qPCR was used to validate differentially expressed genes (DEGs) (ICAM5, GDF15, NECTIN4, SERPINB2) and AS genes (IL24, APEX1, PVT1, HNRNPUL1) regulated by RP11-284N8.3, consistent with transcriptome changes. In summary, RP11-284N8.3 has a significant global regulatory effect in LPS-treated BEAS-2B cells and its possible protective role against sepsis-induced ALI. We propose RP11-284N8.3 and its downstream targets as potential therapeutic targets for sepsis management in the future.
2025-06-12 | GSE299503 | GEO
Project description:Small Noncoding RNAome Changes during macrophage polarization
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Project description:Downregulations of TCAM1P-004 and RP11-598D14.1 were frequently observed in HCC tumors as compared to adjacent non-tumor tissues. To further study the molecular functions of TCAM1P-004 and RP11-598D14.1, we attempted to identify the gene targets regulated by either lncRNAs. Knockdown of TCAM1P-004 or RP11-598D14.1 were achieved by transduction of lentivirus carrying respective shRNAs in non-tumor hepatocyte MIHA cells. Diffferentially expressed genes after knockdown of the lncRNAs were compared to cells tranduced with lentivirus carrying scramble shRNAs.
2018-10-24 | E-MTAB-7280 | biostudies-arrayexpress
Project description:Long noncoding RNAs (lncRNAs) have emerged as novel regulators of macrophage biology and related inflammatory cardiovascular diseases. However, studies focused on lncRNAs in human macrophage subtypes, particularly human lncRNAs that are not conserved in rodents, are limited. Through RNA-seq of human monocyte-derived macrophages, we identified Suppressor of Inflammatory Macrophage Apoptosis lncRNA (SIMALR), a human macrophage-specific long intergenic noncoding RNA, to be highly induced in LPS/IFNγ-stimulated macrophages. Treatment of LPS/IFNγ stimulated THP1 human macrophages with SIMALR antisense oligonucleotides induced apoptosis of inflammatory macrophages, as shown by increased protein expression of cleaved PARP, caspase 9, caspase 3, and Annexin V+. RNA-seq of control versus SIMALR knockdown in LPS/IFNγ-stimulated human monocyte derived macrophages showed NTN1 to be significantly decreased upon SIMALR knockdown. As expected, NTN1 knockdown in LPS/IFNγ-stimulated macrophages induced apoptosis. This apoptotic phenotype was attenuated by adding recombinant NTN1 after SIMALR knockdown. Furthermore, NTN1 promoter-luciferase reporter activity was increased in HEK293T cells treated with lentiviral overexpression of SIMALR. NTN1 promoter activity is known to require HIF1α. RNA immunoprecipitation and microscopy studies suggest that SIMALR may interact with HIF1α to regulate NTN1 transcription, thereby regulating apoptosis of macrophages. In translational studies, SIMALR was found to be expressed in macrophages in human carotid atherosclerotic plaques of symptomatic patients. SIMALR is a non-conserved, human macrophage lincRNA expressed in human atherosclerosis that regulates macrophage apoptosis. SIMALR partners with HIF1α to regulate NTN1, which is a known macrophage survival factor. This work illustrates the importance of interrogating the functions of non-conserved human lincRNAs and exploring their translational and therapeutic potential in human atherosclerosis.
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Project description:GAPLINC is a conserved long noncoding RNA that we find to be highly expressed in macrophages. Inflammatory activation of macrophages results in a decrease in GAPLINC expression, and GAPLINC knockout results in an enhanced expression of inflammatory genes at baseline. To gain insights into the molecular mechanism of GAPLINC, we generated RNA-seq libraries from wild type and GAPLINC-deficient BMDMs untreated and treated with LPS.
2021-02-01 | GSE150574 | GEO