The long non-coding antisense RNA JHDM1D-AS1 regulates inflammatory responses in human monocytes
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA833859 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR19021038.fastq.gz | Fastqsanger.gz | |||
| SRR19021039.fastq.gz | Fastqsanger.gz | |||
| SRR19021040.fastq.gz | Fastqsanger.gz | |||
| SRR19021041.fastq.gz | Fastqsanger.gz | |||
| SRR19021042.fastq.gz | Fastqsanger.gz |
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Project description:Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. In this study, we used RNA sequencing data of circulatory blood monocytes obtained from sepsis patients to identify the elevated antisense lncRNA JHMD1D-AS1, relative to healthy participants. We subsequently demonstrated that in both circulatory blood monocytes and monocyte-derived macrophages exposed to TLR-agonists, JHMD1D-AS1 expression was induced in a temporal specific manner. Using small interfering RNA (siRNA) electroporation to render monocytes deficient of JHDM1D-AS1 and over-expression experiments, we revealed a role for lncRNA JHDM1D-AS1 in cell development, as well as in restraining pro-inflammatory gene expression. Altogether, these findings identify antisense lncRNA JHDM1D-AS1 as a potential repressor of the inflammatory response in human primary monocytes and macrophages.
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Project description:Long non-coding RNA NR2F1 antisense RNA1 (lncRNA NR2F1-AS1) was identified as the main candidate associated to late recurrence in ER-positive breast cancer clinical samples. Gain-of-function of NR2F1-AS1 induced the expression of dormancy-inducers BMP4 and DEC2, and upregulated pluripotency markers NANOG and OCT4. Representative pathways entailed to metastatic events such as HER2/Neu, hypoxia, EMT and inflammatory-response were also found enriched.
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Project description:Monocytes are key players in innate immunity, with their ability to regulate inflammatory responses and combat invading pathogens. There is a growing body of evidence indicating that long non-coding RNA (lncRNA) participate in various cellular biological processes, including the innate immune response. The immunoregulatory properties of numerous lncRNAs discovered in monocytes remain largely unexplored. Here, by RNA sequencing, we identified a lncRNA JHDM1D-AS1, which was upregulated in blood monocytes obtained from patients with sepsis relative to healthy controls. JHDM1D-AS1 expression was induced in primary human monocytes exposed to Toll-like receptor ligands, such as lipopolysaccharide (LPS), or bacteria. The inducibility of JHDM1D-AS1 expression in monocytes depended, at least in part, on nuclear factor-κB activation. JHDM1D-AS1 knockdown experiments in human monocyte-derived macrophages revealed significantly enhanced expression of inflammatory mediators, before and after exposure to LPS, relative to control cells. Specifically, genes involved in inflammatory responses were upregulated (e.g., CXCL2, CXCL8, IL1RN, TREM1, TNF, and IL6), whereas genes involved in anti-inflammatory pathways were downregulated (e.g., SOCS1 and IL10RA). JHDM1D-AS1 overexpression in a pro-monocytic cell line revealed diminished pro-inflammatory responses subsequent to LPS challenge. Collectively, these findings identify JHDM1D-AS1 as a potential anti-inflammatory mediator induced in response to inflammatory stimuli.
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