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RNA sequencing reveals the expression profiles of long noncoding RNA in lipopolysaccharide-induced sepsis

ABSTRACT: RNA sequencing reveals the expression profiles of long noncoding RNA in lipopolysaccharide-induced sepsis

PROVIDER: PRJNA860087 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR20308652_1.fastq.gz	Fastqsanger.gz
	SRR20308652_2.fastq.gz	Fastqsanger.gz
	SRR20308653_1.fastq.gz	Fastqsanger.gz
	SRR20308653_2.fastq.gz	Fastqsanger.gz
	SRR20308654_1.fastq.gz	Fastqsanger.gz

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RNA sequencing reveals the expression profiles of long noncoding RNA in lipopolysaccharide-induced sepsis

Project description:There are currently no specific diagnostic biomarkers and effective pharmacological treatments for sepsis, which makes the mortality rate remains high. Although non-coding RNAs seem to be superior candidates as biomarkers and therapeutics for sepsis, the role of long noncoding RNA (lncRNA) in sepsis remains not completely understood. We then performed gene expression profiling analysis using data obtained from RNA-seq of 2 different cells at the same time point.

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Long noncoding RNA HITT coordinates with RGS2 to inhibit PD-L1 translation in T cell immunity-proteome

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Neutrophils restrain sepsis associated coagulopathy via extracellular vesicles carrying superoxide dismutase 2 in a murine model of lipopolysaccharide induced sepsis

Project description:Disseminated intravascular coagulation (DIC) is a deadly complication of sepsis lacking effective managements. Although excessive inflammatory responses are emerging as key triggers of coagulopathy in sepsis, the interplays between immune system and coagulation are not fully understood. In a murine model of sepsis induced by intraperitoneal lipopolysaccharide (LPS), we found neutrophils in circulation mitigate the occurrence of DIC, thereby preventing the subsequent septic death. We found circulating neutrophils constantly release extracellular vesicles (EVs) containing mitochondria, which carry substantial amount of Superoxide Dismutase 2 (Sod2) upon LPS exposure. The extracellular Sod2 is necessary to bring about neutrophils’ antithrombotic function by eliminating endothelial reactive oxygen species (ROS) accumulation and alleviating endothelial dysfunction. Intervening endothelial ROS accumulation by antioxidants significantly ameliorates DIC with correspondingly improved survival in sepsis. These findings revealed a novel interaction between neutrophils and vascular endothelium which critically regulates coagulation in sepsis and had potential implications for the management of septic DIC.

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Project description:Sepsis is a life-threatening disease that often causes multiple organ dysfunctions. Long noncoding RNAs (lncRNAs) are involved in the pathogenesis and development of sepsis. However, there is little known about the function of lncRNAs in sepsis-induced myocardial dysfunction.To test the hypothesis that dysregulating lncRNAs may be involved in sepsis-induced myocardial dysfunction, we identified differentially expressed (DE) lncRNAs and mRNAs in cardiac tissue by high-throughput sequencing. We constructed coding and non-coding co-expression (CNC) and lncRNA-micro RNA (miRNA)-mRNA competing endogenous networks. The findings will provide useful information for exploring therapeutic candidate targets and new molecular biomarkers of septic myocardial injury.

2023-05-17 | GSE153086 | GEO

Angiogenic patterning by STEEL, an endothelial-enriched long noncoding RNAAngiogenic patterning by STEEL, an endothelial-enriched long noncoding RNA

Project description:Endothelial cell (EC)-enriched protein coding genes, such as endothelial nitric oxide synthase (eNOS), define quintessential EC-specific physiologic functions. It is not clear whether long noncoding RNAs (lncRNAs) also define cardiovascular cell-type specific phenotypes, especially in the vascular endothelium. Here, we report the existence of a set of EC-enriched lncRNAs and define a role for STEEL (spliced transcript – endothelial enriched lncRNA) in angiogenic potential, macrovascular/microvascular identity and shear stress responsiveness. STEEL is expressed from the terminus of the HOXD locus and is transcribed antisense to HOXD transcription factors. STEEL RNA increases the number and integrity of de novo perfused microvessels in an in vivo model and augments angiogenesis in vitro. The STEEL RNA is polyadenylated, nuclear-enriched and has microvascular predominance. Functionally, STEEL regulates a number of genes in diverse endothelial cells. Of interest, STEEL upregulates both eNOS and the transcription factor Kruppel-like factor 2 (KLF2), and is subject to feedback inhibition by both eNOS and shear-augmented KLF2. Mechanistically, STEEL upregulation of eNOS and KLF2 is transcriptionally mediated, in part, via interaction of chromatin-associated STEEL with the poly-ADP ribosylase, PARP1. For instance, STEEL recruits PARP1 to the KLF2 promoter. This work identifies a role for EC-enriched lncRNAs in the phenotypic adaptation of ECs to both body position and hemodynamic forces, and establishes a newer role for lncRNAs in the transcriptional regulation of EC identity.

2018-02-28 | PXD008581 | Pride

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