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Genetic inhibition of CARD9 accelerates the development of experimental atherosclerosis through CD36 dependent-defective autophagy

ABSTRACT: Genetic inhibition of CARD9 accelerates the development of experimental atherosclerosis through CD36 dependent-defective autophagy

PROVIDER: PRJNA916199 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22895235_1.fastq.gz	Fastqsanger.gz
	SRR22895235_2.fastq.gz	Fastqsanger.gz
	SRR22895236_1.fastq.gz	Fastqsanger.gz
	SRR22895236_2.fastq.gz	Fastqsanger.gz
	SRR22895237_1.fastq.gz	Fastqsanger.gz

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Genetic inhibition of CARD9 accelerates the development of experimental atherosclerosis through CD36 dependent-defective autophagy

Project description:Macrophage-mediated innate immune responses contribute to the initiation, progression and complications of atherosclerosis. However, the underlying pathways linking activation of macrophages to atherosclerotic plaque develoment are still poorly understood. We hypothesized that activation of caspase recruitment-domain containing protein 9 (CARD9) plays a determinant role in pro-atherogenic responses in macrophages. Transcriptomic analysis of human monocytes isolated from CARD9-deficient patients confirmed the pathogenic signature identified in several murine models: increased production of pro-inflammatory cytokines, improved lipid uptake, higher cell death susceptibility and defective autophagy.

2023-04-01 | GSE221782 | GEO

Genetic inhibition of CARD9 accelerates the development of atherosclerosis in mice through CD36 dependent-defective autophagy.

Project description:Caspase recruitment-domain containing protein 9 (CARD9) is a key signaling pathway in macrophages but its role in atherosclerosis is still poorly understood. Global deletion of Card9 in Apoe-/- mice as well as hematopoietic deletion in Ldlr-/- mice increases atherosclerosis. The acceleration of atherosclerosis is also observed in Apoe-/-Rag2-/-Card9-/- mice, ruling out a role for the adaptive immune system in the vascular phenotype of Card9 deficient mice. Card9 deficiency alters macrophage phenotype through CD36 overexpression with increased IL-1β production, increased lipid uptake, higher cell death susceptibility and defective autophagy. Rapamycin or metformin, two autophagy inducers, abolish intracellular lipid overload, restore macrophage survival and autophagy flux in vitro and finally abolish the pro-atherogenic effects of Card9 deficiency in vivo. Transcriptomic analysis of human CARD9-deficient monocytes confirms the pathogenic signature identified in murine models. In summary, CARD9 is a key protective pathway in atherosclerosis, modulating macrophage CD36-dependent inflammatory responses, lipid uptake and autophagy.

| S-EPMC10394049 | biostudies-literature

Card9 dependent activation of macrophages by TDB

Project description:Bone marrow derived macrophages from wt and card9 KO mice were stimulated with CpG, Curdlan or TDB, an analogon to the mycobacterial cord factor TDM for 48h, respectively. Keywords: card9 knockout, macropphage, TDB wt or card9 KO macrophages stimulated for 48h

2009-01-31 | E-GEOD-10530 | biostudies-arrayexpress

Card9 protects zymosan-induced peritonitis through regulating autophagy in macrophage

Project description:CARD9 is an adapter protein, which plays a critical role in anti-fungal immunity. However, the role of CARD9 in fungal-induced autophagy remains unknown. In this study, we demonstrated that Card9-/- mice displayed more severe phenotype of zymosan-induced peritonitis, presenting as multiple organs injury and increased systemic inflammation. Moreover, the number of macrophage in spleen was increased in Card9-/- mice. Further studies revealed that autophagy was impaired in peritoneal macrophages of Card9-/- -peritonitis mice. Notably, the autophagy agonist, rapamycin, ameliorated peritonitis in Card9-/- mice. Moreover, Card9 mediates the interaction of Malt1 and P62 upon zymosan stimulation. Together, our results confirmed the protective role of Card9 in the development of peritonitis via regulates autophagy in macrophage cells. The study indicates Card9 may be a potential therapeutic target for peritonitis.

2024-01-01 | GSE164572 | GEO

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60746 | ENA

Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

Project description:Intermittent childhood hyperlipidaemia alters resident arterial macrophages and accelerates atherosclerosis

| PRJEB60780 | ENA

Colon gene expression signatures in wild type and Card9-/-mice exposed to DSS induced colitis

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. For the induction of colitis, mice were given drinking water supplemented with 2% (w/v) Dextran sulphate sodium (DSS) for 7 days, then allowed to recover by drinking water alone for 5 additional days. 3 mice of each groups (WT and Card9-/-) were sacrified before DSS administration. 5 WT mice and 4 Card9-/- mice were sacrified 7 days after DSS administration and 5 mice of each group were sacrified at day 12.

2016-04-05 | E-GEOD-67577 | biostudies-arrayexpress

Card9 dependent activation of macrophages by TDB

2009-02-01 | GSE10530 | GEO

The loss of CARMN regulates vascular smooth muscle cell phenotype and accelerates the development of atherosclerosis in mice.

Project description:We investigated the function of CARMN lncRNA, located immediately upstream of the miRNAs miR-143 and miR-145, as critical regulator of vSMC phenotypes in vitro and the consequence of its loss during the development of atherosclerosis in vivo. We hypothesized that loss of CARMN is a primary event controlling the functional switch towards pro-atherogenic vSMC phenotypes and accelerates the development of the plaques in vivo.

2021-04-06 | GSE158972 | GEO

CARD9 impacts colitis by altering gut microbiota metabolism of tryptophan into aryl hydrocarbon receptor ligands

Project description:It is crucial to decipher the host-microbiota interactions as they are involved in intestinal homeostasis and diseases. Caspase Recruitment Domain 9 (Card9) is an inflammatory bowel disease (IBD) susceptibility gene coding for an adapter protein for innate immunity toward many microorganisms. Card9 mediates colitis recovery via interleukin 22 pathway activation and Card9-/- mice have enhanced susceptibility to colitis. To reveal the mechanisms responsible of this defect in Card9-/-mice, we compared colon transcriptomics in WT and Card9-/- mice before and during DSS-induced colitis. Mice transcriptomes clusterized according to the genotype supporting a pattern clearly different in WT and Card9-/- mice. The number of up-regulated genes at day 7 was largely higher in Card9-/- compared to WT mice. Pathway analyses of the induced transcripts showed a dominance of immune-related pathway with a stronger signal in Card9-/- mice. Interestingly, NOD-like receptor signaling pathway, in which CARD9 is involved, was an exception with weaker activation in Card9-/- than in WT mice. During the recovery period at day 12, pathways involved in cell proliferation and replication were significantly activated in WT compared to Card9-/- mice confirming the healing defect in Card9-/- mice. Results published in Nature Medicine, doi:10.1038/nm.4102

2016-04-05 | GSE67577 | GEO

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