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A conserved long noncoding RNA, GAPLINC, modulates the immune response during endotoxic shock

ABSTRACT: A conserved long noncoding RNA, GAPLINC, modulates the immune response during endotoxic shock

PROVIDER: PRJNA632850 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11790200.fastq.gz	Fastqsanger.gz
	SRR11790200_1.fastq.gz	Fastqsanger.gz
	SRR11790200_2.fastq.gz	Fastqsanger.gz
	SRR11790201.fastq.gz	Fastqsanger.gz
	SRR11790201_1.fastq.gz	Fastqsanger.gz

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A conserved long noncoding RNA, GAPLINC, modulates the immune response during endotoxic shock

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.

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A conserved long noncoding RNA, GAPLINC, modulates the immune response during endotoxic shock.

Project description:Recent studies have identified thousands of long noncoding RNAs (lncRNAs) in mammalian genomes that regulate gene expression in different biological processes. Although lncRNAs have been identified in a variety of immune cells and implicated in immune response, the biological function and mechanism of the majority remain unexplored, especially in sepsis. Here, we identify a role for a lncRNA-gastric adenocarcinoma predictive long intergenic noncoding RNA (GAPLINC)-previously characterized for its role in cancer, now in the context of innate immunity, macrophages, and LPS-induced endotoxic shock. Transcriptome analysis of macrophages from humans and mice reveals that GAPLINC is a conserved lncRNA that is highly expressed following macrophage differentiation. Upon inflammatory activation, GAPLINC is rapidly down-regulated. Macrophages depleted of GAPLINC display enhanced expression of inflammatory genes at baseline, while overexpression of GAPLINC suppresses this response. Consistent with GAPLINC-depleted cells, Gaplinc knockout mice display enhanced basal levels of inflammatory genes and show resistance to LPS-induced endotoxic shock. Mechanistically, survival is linked to increased levels of nuclear NF-κB in Gaplinc knockout mice that drives basal expression of target genes typically only activated following inflammatory stimulation. We show that this activation of immune response genes prior to LPS challenge leads to decreased blood clot formation, which protects Gaplinc knockout mice from multiorgan failure and death. Together, our results identify a previously unknown function for GAPLINC as a negative regulator of inflammation and uncover a key role for this lncRNA in modulating endotoxic shock.

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Inhibition of netosis with PAD inhibitor attenuates endotoxin shock induced systemic inflammation

Project description:Neutrophils play a pivotal role in innate immunity and participate in a range of immunological disorders. Excessive neutrophil extracellular traps formed at infection and tissue damage sites are detrimental to the local tissue and further exacerbate inflammation. Protein arginine deiminases mediate histone citrullination and NET formation thereby regulating endotoxin shock response. However, the molecular mechanisms are less known. Here we report that inhibition of netosis attenuates inflammation in a LPS induced lethal endotoxic shock model in mice. Albeit a higher number of neutrophils are accumulated in peritoneal cavity the primary inflammatory site, the level of inflammatory signals is greatly reduced after netosis inhibition with a PAD inhibitor. In lungs under endotoxic stress, gene expression analyses indicate that LPS induced a drastic increase in inflammatory gene expression. In contrast, lung tissue damage and inflammation were much reduced after PAD inhibition to reduce netosis. In summary, we found NET formation inhibition as a new avenue to manage inflammatory damages under endotoxic stress.

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