ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2021
C/EBPβ is a key transcription factor of ox-LDL inducing THP-1 cells to release multiple pro-inflammatory cytokines.
Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers, 2 of them syntheses that pooled it.
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Who cites it
9 citing papers in PubMed, 2 syntheses or guidelines pooled it, 12 citations in OpenAlex.
- C/EBPβ as a master regulator of inflammasome signaling in neurodegenerative diseases: mechanisms and therapeutic implications.Frontiers in immunology · 2025Pooled it
- C/EBPβ: A transcription factor associated with the irreversible progression of Alzheimer's disease.CNS neuroscience & therapeutics · 2024Pooled it
- IL-18 binding protein attenuates neuroinflammation and cognitive decline in Alzheimer's disease.Journal of neuroinflammation · 2026Article
- C/EBPβ activation in vascular smooth muscle cells promotes hyperlipidemia-induced phenotypic transition and arterial stiffness.Signal transduction and targeted therapy · 2025Article
- Overexpression of Neural Precursor Cell Expressed Developmentally Downregulated 9 (NEDD9) reduces ox-LDL-induced Anoikis in atherosclerotic vascular endothelial cells.International journal of cardiology. Heart & vasculature · 2025Article
- Article
- Association between atherosclerosis and the development of multi-organ pathologies.SAGE open medicine · 2024Review
- Investigation of LGALS2 expression in the TCGA database reveals its clinical relevance in breast cancer immunotherapy and drug resistance.Scientific reports · 2023Article
- C/EBPβ Promotes LPS-Induced IL-1β Transcription and Secretion in Alveolar Macrophages via NOD2 Signaling.Journal of inflammation research · 2022Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
objectiveCCAAT/enhancer binding protein β (C/EBPβ) plays an important role during atherogenesis. However, how C/EBPβ functions remains unclear. In this study, we explore the relationship between C/EBPβ and oxidized LDL-induced multiple pro-inflammatory cytokines released in monocytes. MATERIALS AND
methodsTHP-1 cells (human monocyte cell line) were stimulated by ox-LDL, ChIP was used to detect the binding function of C/EBPβ to target genes, small interfering RNA was used to knock down the expression of C/EBPβ, Western Blot was used to detect protein expression, and ChIP-seq was used to detect different groups of C/EBPβ bound gene fragments. The integrative genomics viewer (IGV), model-based analysis of ChIP-seq (MACS) were used to visualize the results of ChIP-seq. GO (gene ontology), KEGG (Kyoto Encyclopedia of Genes and Genomes) and Reactome data bases enrichment analysis were performed by the ClusterProfiler software. Ingenuity pathway analysis (IPA) was used to analyze the results of ChIP-seq and to summarize the data within the database.
resultsWe identified C/EBPβ as a key protein that regulated IL-1β, IL-6 through database. Then our results confirmed that C/EBPβ could bind directly to the gene of IL-18 and C/EBPβ plays a role in the increased expression and secretion of IL-18 protein after ox-LDL stimulation of THP-1. Using ChIP-seq, we found that the enhanced transcriptional function of C/EBPβ after ox-LDL treatment triggered changes in C/EBPβ-regulated downstream pathways. In the ChIP-seq results, we extracted inflammatory cytokines with significant expression differences, and by comparing them with the database of inflammatory cytokines that C/EBPβ directly regulated, we screened five inflammatory cytokines, CXCL8, IL17B, TNFSF11, CSF3, and CCL2, and the results showed that knockdown of C/EBPβ expression inhibited ox-LDL-induced secretion of CXCL8, TNFSF11, CSF3, and CCL2 by THP-1.
conclusionOur results suggest that ox-LDL stimulation enhances C/EBPβ-regulated transcription in THP-1 and C/EBPβ upregulate the release of multiple pro-inflammatory cytokines including IL-18, IL-1β, and IL-6 through direct binding to genes.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.