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Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

ABSTRACT: Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

PROVIDER: PRJNA1033370 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26558506_1.fastq.gz	Fastqsanger.gz
	SRR26558506_2.fastq.gz	Fastqsanger.gz
	SRR26558507_1.fastq.gz	Fastqsanger.gz
	SRR26558507_2.fastq.gz	Fastqsanger.gz
	SRR26558508_1.fastq.gz	Fastqsanger.gz

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Lipolysis Engages CD36 to Promote ZBP1-Mediated Necrosis Impairing Lung Regeneration in COPD

Project description:Lung parenchyma destruction represents a severe condition commonly found in chronic obstructive pulmonary disease (COPD), the leading cause of morbidity and mortality worldwide. Promoting lung regeneration is crucial for achieving clinical improvement. However, no therapeutic drugs are approved to improve the regeneration capacity due to incomplete understanding of the underlying pathogenic mechanisms. Here, we identify a positive feedback loop formed between adipose triglyceride lipase (ATGL)-mediated lipolysis and overexpression of CD36 specific to lung epithelial cells, contributing to disease progression. Genetic deletion of CD36 in lung epithelial cells and pharmacological inhibition of either ATGL or CD36 effectively reduce COPD pathogenesis and promote lung regeneration in mice. Mechanistically, disruption of the ATGL-CD36 loop rescued Z-DNA binding protein 1 (ZBP1)-induced cell necroptosis and restored WNT/β-catenin signaling. Thus, we uncover a previously unrecognized crosstalk between lipolysis and lung epithelial cells, suggesting the regenerative potential for therapeutic intervention by targeting the ATGL-CD36-ZBP1 axis in COPD.

2024-12-13 | GSE246501 | GEO

Lipolysis engages CD36 to promote ZBP1-mediated necroptosis-impairing lung regeneration in COPD.

Project description:Lung parenchyma destruction represents a severe condition commonly found in chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality worldwide. Promoting lung regeneration is crucial for achieving clinical improvement. However, no therapeutic drugs are approved to improve the regeneration capacity due to incomplete understanding of the underlying pathogenic mechanisms. Here, we identify a positive feedback loop formed between adipose triglyceride lipase (ATGL)-mediated lipolysis and overexpression of CD36 specific to lung epithelial cells, contributing to disease progression. Genetic deletion of CD36 in lung epithelial cells and pharmacological inhibition of either ATGL or CD36 effectively reduce COPD pathogenesis and promote lung regeneration in mice. Mechanistically, disruption of the ATGL-CD36 loop rescues Z-DNA binding protein 1 (ZBP1)-induced cell necroptosis and restores WNT/β-catenin signaling. Thus, we uncover a crosstalk between lipolysis and lung epithelial cells, suggesting the regenerative potential for therapeutic intervention by targeting the ATGL-CD36-ZBP1 axis in COPD.

| S-EPMC11525022 | biostudies-literature

ZBP1 is a cytosolic RNA virus sensor driving activation of the NLRP3 inflammasome, pyroptosis, necroptosis and apoptosis

Project description:The innate immune system recognizes nucleic acids as a signature of microbial infection and initiates host-protective responses, including the production of type I IFN and proinflammatory cytokines. Z-DNA binding protein 1 (ZBP1, also known as DLM-1 or DAI) was previously identified as a dsDNA binding protein, triggering DNA-mediated activation of innate immune responses. However, mice or cells lacking ZBP1 produce normal levels of type I IFN in response to dsDNA. Therefore, the classification of ZBP1 as a true DNA sensor remains to be resolved. Here, we report that the single stranded RNA virus, influenza A virus (IAV) is a trigger of the cytosolic sensor ZBP1. Sensing of IAV infection by ZBP1 engages a novel NLRP3 inflammasome pathway that is not defined by the conventions of the canonical and non-canonical NLRP3 inflammasome pathways. Surprisingly, IAV-induced cell death was not prevented by the absence of the NLRP3 inflammasome. Instead, we identified parallel contributions from pyroptosis, necroptosis and apoptosis in the execution of ZBP1-dependent cell death, mediated by the kinase RIPK3. Overall, the ability of ZBP1 to sense IAV infection signifies a point of divergence for IAV-induced programmed cell death pathways and inflammasome activation. We used microarrays to explore the gene expression profiles differentially expressed in influenza-infected bone marrow derived macrophages (BMDM) isolated from Ifnar1-/- and wild-type mice.

2016-08-11 | E-GEOD-77611 | biostudies-arrayexpress

Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation via CD36

Project description:Lipolysis-derived linoleic acid drives beige fat progenitor cell proliferation via CD36

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Expression data from ZBP1-expression and ZBP1 nonexpression breast tumors.

Project description:ZBP1/IMP1 is an mRNA binding protein that post-transcriptionally regulates the expression of a handful mRNAs, implicated in maintaining cell polarity and adhesion. We have previously shown that ZBP1 was able to inhibit proliferation and invasiveness of breast carcinoma cells in vitro. In the current study, we utilized orthotopic breast fat pad xenografts to further investigate the ZBP1-mediated functions in breast tumorigenesis and metastasis in vivo. We used microarrays to identify important gene for breast tumor growth and metastasis in response to ZBP1 expression Total RNA was extracted from breast tumor generated from ZBP1-expression and ZBP1-nonexpression MDA231 cells and used for hybridization on Affymetrix microarrays. We sought to obtain gene expression profiles from the individual tumors and identify what genes are up-regulated or down-regulated in the presence of ZBP1. The microarray experiments and data analysis were performed in 'Gene Company Limited' in Senzheng, China. G-10 and G-13, Tumors generated from MDA231/GFP cells; I-5 and I-6, tumors generated from MDA231/ZBP1-GFP cells.

2014-10-24 | E-GEOD-62638 | biostudies-arrayexpress

ZBP1 is a cytosolic RNA virus sensor driving activation of the NLRP3 inflammasome, pyroptosis, necroptosis and apoptosis

2016-08-11 | GSE77611 | GEO

Effcts of Zbp1 in B-cell lymphoma

Project description:B-cell lymphomas arising in Zbp1-/-Eu-Myc mice were compared to B-cell lymphomas arising in Zbp1+/+Eu-Myc mice

2014-04-01 | E-MTAB-2354 | biostudies-arrayexpress

Expression data from ZBP1-expression and ZBP1 nonexpression breast tumors.

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Transcriptomic analysis of WT, Tfam+/-, Zbp1-/- and Tfam+/-Zbp1-/- mouse embryonic fibroblasts (MEFs)

Project description:The goal of this study was to compare the gene expression profiles of WT, Tfam+/-, Zbp1-/- and Tfam+/-Zbp1-/- MEFs.

2023-01-28 | GSE223553 | GEO

IRF3 and ZBP1