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Bulk RNA-seq of wild-type and Nlrp3-/- bone marrow-derived macrophages with or without LPS and ATP costimulation

ABSTRACT: Bulk RNA-seq of wild-type and Nlrp3-/- bone marrow-derived macrophages with or without LPS and ATP costimulation

PROVIDER: PRJNA1209897 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR31978628_1.fastq.gz	Fastqsanger.gz
	SRR31978628_2.fastq.gz	Fastqsanger.gz
	SRR31978629_1.fastq.gz	Fastqsanger.gz
	SRR31978629_2.fastq.gz	Fastqsanger.gz
	SRR31978630_1.fastq.gz	Fastqsanger.gz

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Bulk RNA-seq of wild-type and Nlrp3-/- bone marrow-derived macrophages with or without LPS and ATP costimulation

Project description:In order to investigate the effect of NLRP3 on the transcription profile of inactive macrophages and active macrophages with LPA and ATP combined stimulation.

2025-01-20 | GSE286554 | GEO

Acetylomics on rhein treated NLRP3 activated J774A.1 macrophages

Project description:The aim of this project is to observe the effect of 5 μM rhein treatment on the acetylation level of NLRP3 activated macrophages. We primed J774A.1 cells with 100ng/mL LPS for 12 hours followed by 5μM rhein treatment for 30 minutes. Finally, the cells were stimulated with 4 mM ATP for 30 min to trigger the inflammasome assembly. Cell lysates were collected after ATP stimulation by cell scrapers, and acetylomics were performed as described below.

2024-10-17 | PXD044992 | Pride

Mitochondrial electron transport chain is necessary for NLRP3 inflammasome activation

Project description:The NLRP3 inflammasome is linked to sterile and pathogen-dependent inflammation, and its dysregulation underlies many chronic diseases. Mitochondria have been implicated as regulators of NLRP3 inflammasome through multiple mechanisms including generation of mitochondrial ROS. Here we report that mitochondrial electron transport chain (ETC) complexes I, II, III and V inhibitors all prevent NLRP3 inflammasome activation. Ectopic expression of Saccharomyces cerevisiae NADH dehydrogenase (NDI1) or Ciona intestinalis alternative oxidase (AOX), which can respectively complement the functional loss of mitochondrial complex I or III, without generation of ROS, rescued NLRP3 inflammasome activation in the absence of endogenous mitochondrial complex I or complex III function. Metabolomics revealed phosphocreatine (PCr), which can sustain ATP levels, as a common metabolite that is diminished by mitochondrial ETC inhibitors. PCr depletion decreased ATP levels and NLRP3 inflammasome activation. Thus, mitochondrial ETC sustains NLRP3 inflammasome activation through PCr-dependent generation of ATP but a ROS independent mechanism.

2022-03-09 | GSE197606 | GEO

Inhibition of GGPPS1 attenuated LPS-induced acute lung injury by suppressing the NLRP3 inflammasome

Project description:Rationale: Geranylgeranyl pyrophosphate synthase large subunit 1 (GGPPS1), a catalase downstream of the mevalonate pathway, regulates various pathological processes through balancing the production of farnesyl pyrophosphate and geranylgeranyl pyrophosphate. We sought to investigate whether GGPPS1 plays a role in mediating acute lung injury (ALI) using a mouse model of inflammation. Methods: Lipopolysaccharide (LPS) was intra-tracheally instilled to induce ALI in lung specific GGPPS1 knockout and wild-type mice. Expression of GGPPS1 in lung tissues and alveolar epithelial cells (AECs) was examined at different time points. Alveolar exudate, neutrophil infiltration, lung injury and cell death were determined. Change in global gene expression in response to GGPPS1 depletion was measured using mRNA microarray and verified in vivo and in vitro. Results: GGPPS1 levels increased significantly in lung tissues from LPS-induced ALI mice, where it showed a time- and dose-dependent increase in alveolar epithelial cells. Specific deletion of pulmonary GGPPS1 reduced the alveolar exudate and attenuated the severity of lung injury through inhibiting apoptosis of AECs. However, GGPPS1 deletion had limited effect on neutrophil counts and TNF-α levels in alveolar fluids. Deletion of GGPPS1 inhibited LPS-induced inflammasome activation, in terms of IL-1β release and pyroptosis, by down-regulating NLRP3 expression. Conclusions: Inhibition of pulmonary GGPPS1 attenuated LPS-induced ALI, predominantly by suppressing NLRP3 inflammasome activation.

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Tyrosine Phosphorylation of NLRP3 by Src Family Protein Tyrosine Kinase Lyn Suppresses NLRP3 Inflammasome Activation

Project description:The NLRP3 inflammasome is a multi-protein complex that triggers the activation of the inflammatory protein caspase-1 and the maturation of the cytokine IL-1 in response to microbes and other danger signals in host cells. Here, we sought a deeper understanding of how the NLRP3 inflammasome is regulated. We found that inflammasome activation induced the Src family kinase Lyn to phosphorylate NLRP3 at Tyr918, and that this phosphorylation of NLRP3 correlated with a subsequent increase in its ubiquitination, which facilitated its proteasome-mediated degradation. NLRP3 tyrosine phosphorylation and ubiquitination was abrogated in Lyn-deficient macrophages, which produced increased amounts of IL-1. Furthermore, mice lacking Lyn were highly susceptible to LPS-induced septic shock in an NLRP3-dependent manner. Our data demonstrate that Lyn-mediated tyrosine phosphorylation of NLRP3 is a prerequisite for its ubiquitination, thus dampening NLRP3 inflammasome activity.

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2021-07-26 | GSE180707 | GEO

The role of NLRP3 in intra-amniotic inflammation-induced preterm birth

Project description:Macrophages and neutrophils were sorted from the decidua and uterus of Nlrp3+/+ and Nlrp3-/- mice injected with lipopolysaccharide (LPS) or PBS and analyzed using pair-end RNA-sequencing (RNA-seq) to evaluate the effect of Nlrp3 deficiency on the transcriptomes of these innate immune cells in preterm birth.

2021-12-01 | GSE183698 | GEO

microRNA Expression Changes in Organotin-Driven NLRP3 Inflammasome Activation in Murine Bone Marrow Derived Macrophages

Project description:Trimethyltin (TMT) and triethyltin (TET) are two tri-organotin compounds, a group of substances reported to affect mitochondria function. These compounds were also found to activate the NLRP3 inflammasome, an inflammatory cascade that occurs in myeloid cells when primed with a Toll-like receptor ligand (i.e. LPS) followed by activation by an exogenous or endogenous danger signal. The inflammasome is a very tightly regulated mechanism, with several miRNAs playing an important role. To determine differential miRNA changes between TMT and TET induced inflammasome activation, miRNA expression profiles were evaluated in LPS-primed murine bone marrow derived macrophages (BMDMs) exposed to TMT or TET as compared to saline. mRNA expression arrays were also performed and analyzed to identify miRNA target genes in order to elucidate the key mechanism(s) by which TMT and TET activate the NLRP3 inflammasome pathway. These studies will help us understand the inflammasome regulation in macrophages by organotin.

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mRNA Expression Changes in Organotin-Driven NLRP3 Inflammasome Activation in Murine Bone Marrow Derived Macrophages

2021-05-05 | GSE155126 | GEO

LPS & ATP Stimulated wild type and miR-155 KO murine C57BL/6 Dendritic Cells

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2015-07-30 | E-MTAB-2608 | biostudies-arrayexpress

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