Expression data of C.pn treated foam cell
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PROVIDER: PRJNA471803 | ENA |
REPOSITORIES: ENA
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Project description:C.pn potentiated hyperlipidemia-induced inflammasome activity in cultured macrophages and in foam cells in atherosclerotic lesions of Ldlr–/– mice. We discovered that C.pn-induced extracellular IL-1β triggers a negative feedback loop to inhibit GPR109a and ABCA1 expression and cholesterol efflux leading to accumulation of intracellular cholesterol and foam cell formation. Gpr109a and Abca1 were both upregulated in plaque lesions in Nlrp3–/– mice in both hyperlipidemic and C.pn infection models. We sued microarrays to detail the gene expression underlying C.pn and ox-LDL treatment on mice periteneal macrophages to study the regulating of ABCA1 related genes with NLRP3 manutation
2018-05-18 | GSE114565 | GEO
Project description:Background: Cardiovascular diseases remain the leading cause of morbidity and mortality worldwide, most of which are caused by atherosclerosis. Discerning processes that participate in macrophage-to-foam cell formation are critical for understanding the basic mechanisms underlying atherosclerosis. To explore the molecular mechanisms of foam cell formation, the differentially expressed proteins were identified. Methods: In this paper, human monocytes, macrophage colony-stimulating factor induced macrophages, and oxidized low-density lipoprotein induced foam cells were cultured, and tandem mass tag (TMT) labeling combined with mass spectrometry (MS) were performed to find associations between foam cell transformation and proteome profiles. Results: Totally, 5146 quantifiable proteins were identified, among which 1515 and 182 differentially expressed proteins (DEPs) were found in macrophage/monocyte and foam cell/macrophage, respectively, using a cutoff of 1.5-fold change. Subcellular localization analysis revealed that downregulated DEPs of macrophages/monocytes were mostly located in the nucleus and upregulated DEPs of foam cells/macrophages mostly located in the plasma membrane and extracellular. Functional analysis of DEPs demonstrated that cholesterol metabolism related proteins were upregulated in foam cells, whereas the immune response-related proteins were downregulated in foam cells. The protein-interaction network showed that the DEPs with the highest interaction intensity between macrophages and foam cells were mainly concentrated in lysosomes and the endoplasmic reticulum. Conclusions: This study for the first time to perform quantitative proteomic investigation by TMT labeling and LC-MS/MS to identify differentially expressed proteins in human monocyte, macrophage, and foam cell. The results confirmed cholesterol metabolism was upregulated in foam cells, while immune response was suppressed, which suggested that foam cells were not the population that promote inflammation. In addition, KEGG enrichment analysis and protein-protein interaction indicated that the differentially expressed proteins locating in the endoplasmic reticulum and lysosomes may be key targets to regulate foam cell formation. These data provide a basis for identifying the potential proteins associated with the molecular mechanism involved in the transformation of macrophages to foam cells.
2022-02-15 | PXD028363 | Pride
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Project description:Foam cells are dysfunctional, lipid-laden macrophages associated with chronic inflammation of infectious and non-infectious origin. To test the hypothesis that foam cell biogenesis is disease-specific, we compared bulk transcriptomics data obtained by RNA seq in human monocyte derived macrophages (MDM) subjected to two types of infections in vitro. One was with Mycobacterium tuberculosis and the other with Cryptococcus neoformans. We also exposed MDM to cell-free conditioned medium from cultures of the ACHN cell line, which is derived from a human renal cell carcinoma, to study foam cell formation in the context of papillary renal cell carcinoma (pRCC). We found that, with both infections, the accumulation of TAG results from decreased oxidative phosphorylation, increased glycolysis, increased lipid biosynthesis, and decreased lipid catabolism. However, the molecular modalities of
2025-07-09 | GSE236100 | GEO
Project description:To investigate the intrinsic causes of the high prevalence of atherosclerosis in diabetic patients, we cultured macrophages differentiated from THP-1 in a high-glucose environment and oxidized low-density lipoprotein to induce its transformation into foam cells. We sought the effect of high glucose on gene expression during foam cell formation by transcriptome sequencing.
2023-04-20 | GSE201105 | GEO
Project description:Objective: Foam cells, predominantly originating from vascular smooth muscle cells (VSMCs) and macrophages, are a hallmark of atherosclerotic plaque development. Strategies aimed at inhibiting foam cell formation have emerged as pivotal for atherosclerosis (AS) prevention and therapy. Homocysteine (Hcy), recognized as an independent risk factor for AS, has been shown to trigger the phenotypic transition of VSMCs into foam cells; however, the molecular mechanisms underlying this process remain incompletely elucidated. The present study aimed to identify crucial regulatory proteins and elucidate the mechanistic pathways involved in Hcy-induced foam cell formation from VSMCs, thereby offering a theoretical framework for AS intervention. Methods: VSMCs were allocated into two groups: a control cohort and a group exposed to Hcy to simulate an AS-like state. Quantitative proteomic profiling was performed using 4D Fast-DIA approach to detect differentially expressed proteins between these groups. To explore functional implications, enrichment analyses involving Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways were conducted. Protein-protein interaction networks were constructed using the STRING database to identify central interactors. Target proteins were subsequently validated through parallel reaction monitoring (PRM). Furthermore, histological analyses including hematoxylin and eosin (HE) staining, Oil Red O staining, Western blot, and biochemical analysis were utilized to confirm the role and mechanism of identified proteins in the context of Hcy-driven foam cell conversion. Results: Proteomic analysis identified 4804 proteins, with 4799 proteins being quantitatively comparable. A total of 54 proteins displayed significant differential expression based on thresholds of p < 0.05 and fold change > 1.5 or < 1/1.5. Among them, 13 proteins were upregulated, while 41 were downregulated in response to Hcy treatment. PRM validation focused on 16 candidate proteins: COX7C, STX5, UBQLN2, DDX50, TBCB, GSR, PCNP, CDV3, PEBP1, PPIA, S100A6, EIF4E2, UBQLN1, ARMC1, NUDCD2, and H1-2. Histological staining demonstrated enhanced lipid accumulation and morphological changes indicative of foam cell transformation in Hcy-treated VSMCs. The protein levels of COX7C, and sterol regulatory element-binding proteins (SREBP1C and SREBP2) were elevated upon Hcy exposure. Overexpression of COX7C further augmented the expression of SREBP1C and SREBP2, exacerbated lipid accumulation, and promoted foam cell transformation in Hcy-treated VSMCs. On the other hand, knockdown of COX7C had the opposite effects. Conclusion: COX7C serves as a central regulatory protein in Hcy-induced transformation of VSMCs into foam cells. Its pathogenic role is likely mediated through the upregulation of SREBP1C and SREBP2, thereby promoting lipid accumulation. These findings provide new insights into AS pathogenesis and identify COX7C as a potential therapeutic target.
2026-02-16 | PXD064315 | Pride
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