C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [DC]
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1027330 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR26368600_1.fastq.gz | Fastqsanger.gz | |||
| SRR26368600_2.fastq.gz | Fastqsanger.gz | |||
| SRR26368601_1.fastq.gz | Fastqsanger.gz | |||
| SRR26368601_2.fastq.gz | Fastqsanger.gz | |||
| SRR26368602_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 12 |
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Project description:C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development
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Project description:C1Q+macrophage interacts with activated CD8+ promoting atherosclerosis development [T cell]
| PRJNA1029556 | ENA
Project description:To investigate how DC cells treated with SPI1 inhibitor (DB2313) affected the function of primary T cells. We then performed gene expression profiling analysis using data obtained from RNA-seq of primary T cells incubated with DC cells.
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Project description:To investigated how SPI1 inhibitor (DB2313) affected the function of DCs , we treated BMDM derived DCs,with DB2313. We then performed gene expression profiling analysis using data obtained from RNA-seq of peritoneal DCs with DB2313
2024-05-29 | GSE245183 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2024-05-29 | GSE245667 | GEO
Project description:Atherosclerosis, the underlying vascular cause of cardiovascular disease, has a strong inflammatory component. The co-stimulatory CD40-CD40 ligand (CD40L) signaling axis is a pivotal regulator of immune responses in atherosclerosis. However, therapeutic long-term inhibition of CD40L will severely compromise the immune system making it a non-viable treatment option. To circumvent this issue, cell-specific inhibition may present a better approach to target the CD40-CD40L axis. Therefore, we generated T cell and platelet-specific knockout mice for CD40L and apolipoprotein E, which were aged for 28 weeks to study their effects on immune status and atherosclerosis. Here, we show that T cell specific deficiency in CD40L signaling reduced plaque progression through hampered Th1 polarization as well as reduced antigen-dependent proliferation and oxLDL IgM production. DC-specific CD40 deficient mice displayed a similar phenotype. Platelet-specific CD40L deficiency, however, failed to decrease atherosclerosis, but ameliorated atherothrombosis. Together, our results illuminate the divergent cell-specific mechanisms of CD40-CD40L signaling in atherosclerosis, which may lead to advances in targeted therapies.
2021-03-16 | GSE145585 | GEO
Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12). Bone marrow derived macrophages or J774 cells were adhered to heat inactivated C1q, C1q tails or C1q for 18 hours. Cells were harvested and RNA was isolated and converted to double stranded cDNA and subsequently labeled and hybridized onto NimbleGen mouse gene expression array [100718_MM9_EXP] using Nimblegen Hybridization system 4 according to manufacturerM-bM-^@M-^Ys instructions (Roche)
2014-07-10 | E-GEOD-48619 | biostudies-arrayexpress
Project description:Neuroimmune interactions mediate intercellular communication and underlie critical brain functions. Microglia, CNS-resident macrophages, modulate the brain through direct physical interactions and the secretion of molecules. One such secreted factor, the complement protein C1q, contributes to complement-mediated synapse elimination in development and disease models, yet brain C1q protein levels increase significantly throughout aging. How age-related C1q affects neuronal function has not been demonstrated. Here we report that C1q interacts with neuronal ribonucleoprotein (RNP) complexes in an age-dependent manner. Purified C1q protein undergoes RNA-dependent liquid-liquid phase separation (LLPS) in vitro, and the interaction of C1q with neuronal RNP complexes in vivo is dependent on RNA and endocytosis. Mice lacking C1q have age-specific alterations in neuronal protein synthesis in vivo and impaired fear memory extinction. Together, our findings reveal a biophysical property of C1q that underlies RNA- and age-dependent neuronal interactions and demonstrate a unique role of C1q in critical intracellular neuronal processes.
2024-07-01 | PXD052189 | Pride
Project description:We have data from a previous microarray experiment which shows that C1q elicits macrophages to express genes important for clearance of dead (apoptotic) cells. In this experiment we want to determine the signaling mechanism by which C1q is turning on macrophage gene expression. For our control (sample 1-3) we heated C1q to denature it so it is inactive. We also want to know which portion of C1q is responsible for activation the macrophage so we generated C1qtails (samples 4-5). We also have macrophages treated with the whole C1q molecule (7-9). And finally we have a cell line (J774) treated with C1q but does not activate the cells (samples 10-12).
2014-07-10 | GSE48619 | GEO
Project description:BACKGROUND: Mitochondrial dysfunction is a key factor in the development of atherogenesis. Methyltransferase-like protein 4 (METTL4) mediates N6-deoxyadenosine (6mA) methylation of mammalian mitochondrial DNA (mtDNA). However, the role of METTL4-mediated mitoepigenetic regulation in atherosclerosis is still unknown. This study aims to investigate the potential involvement of METTL4 in atherosclerosis, explore the underlying mechanism, and develop targeted strategies for treating atherosclerosis. METHODS: Expression levels of mtDNA 6mA and METTL4 were determined in atherosclerotic lesions. We explored the mechanism of METTL4 involvement in atherosclerosis using Mettl4Mac-KO-Apoe-/- and Mettl4MUT-Apoe-/- mice and cell models, as well as bone marrow transplantation. Natural compound libraries were screened to identify potent METTL4 antagonists. In addition, bioinspired proteolysis-targeting (PROTAC) technology targeting macrophages within plaques was used to increase the efficacy of the METTL4 antagonist. RESULTS: The expression levels of mtDNA 6mA and METTL4 were significantly increased in plaque macrophages. Mettl4Mac-KO-Apoe-/- mice displayed suppressed mtDNA 6mA levels and atherosclerotic progression, which were reversed by METTL4 restoration via bone marrow transplantation (n = 6). Mechanistically, elevated METTL4 expression reduces MT-ATP6 expression by suppressing its transcription, thereby impairing the activity of mitochondrial respiration chain complex V. This disruption leads to the accumulation of excess protons in the mitochondrial intermembrane space, causing mitochondrial dysfunction. Consequently, mtDNA is released into the cytoplasm, ultimately triggering inflammasome activation. All results were reversed by the mutation in the METTL4 methyltransferase active site. Mettl4MUT-Apoe-/- mice showed suppressed mtDNA 6mA levels and atherosclerotic progression, and repaired mitochondrial function of macrophage, which were reversed by METTL4 restoration via bone marrow transplantation (n = 6). Pemetrexed (PEM) was identified as the first METTL4 antagonist to effectively alleviate atherosclerotic progression. Furthermore, we generated a proteolysis-targeting chimera drug based on PEM (PROTAC-PEM) that specifically targeting METTL4 in macrophages within plaques, showing a promising therapeutic effect on atherosclerosis. CONCLUSIONS: This study revealed a novel mechanism by which mtDNA 6mA orchestrated mitochondrial function-related gene expression in macrophages, thereby promoting atherosclerosis. Through various experimental techniques, such as gene manipulation, pharmacological inhibition and PROTAC, this study demonstrated that mtDNA 6mA and its specific enzyme METTL4 hold potential as therapeutic targets for atherosclerosis.
2024-11-02 | GSE280434 | GEO