Bulk RNA-seq of wild-type and Nlrp3-/- bone marrow-derived macrophages with or without LPS and ATP costimulation
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ABSTRACT:
PROVIDER: PRJNA1209897 | ENA |
REPOSITORIES: ENA
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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.
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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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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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