ArticleJournal of cellular physiology2015
Transcription factor MEF2C suppresses endothelial cell inflammation via regulation of NF-κB and KLF2.
Article in Journal of cellular physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 2 of them syntheses that pooled it.
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Who cites it
46 citing papers in PubMed, 2 syntheses or guidelines pooled it, 67 citations in OpenAlex.
- Genetic Variability in Molecular Pathways Implicated in Alzheimer's Disease: A Comprehensive Review.Frontiers in aging neuroscience · 2021Pooled it
- Finding lost genes in GWAS via integrative-omics analysis reveals novel sub-networks associated with preterm birth.Human molecular genetics · 2016Pooled it
- KLF transcription factors in metabolic kidney disease: from podocyte protection to tubulointerstitial fibrosis.International urology and nephrology · 2026Review
- Dynamic cellular programs of human cardiac allograft rejection revealed by spatial transcriptomics.Nature cardiovascular research · 2026Article
- A MEF2C transcription factor network regulates proliferation of glomerular endothelial cells in diabetic kidney disease.Kidney international · 2026Article
- Exploratory study of dialysis membrane impact on epigenetic methylation patterns in hemodialysis patients using genomic and synchrotron investigations.Scientific reports · 2026Article
- Epigenome-Wide Association Study in Asian Cohort Identifies Novel DNA Methylation Markers for Carotid Intima-Media Thickness.Research square · 2026Article
- Gram-negative bacterial outer membrane proteins and lipopolysaccharides key factors linking chicken coop environment and oxidative stress.Redox biology · 2026Review
- Article
- Epigenome-Wide Association Study in Asian Cohort Identifies Novel DNA Methylation Markers for Carotid Intima-Media Thickness.medRxiv : the preprint server for health sciences · 2025Article
- Transcriptome Insights into Protective Mechanisms of Ferroptosis Inhibition in Aortic Dissection.International journal of molecular sciences · 2025Article
- Plasma-derived extracellular vesicles prime alveolar macrophages for autophagy and ferroptosis in sepsis-induced acute lung injury.Molecular medicine (Cambridge, Mass.) · 2025Article
- Silencing epileptic storms: targeting miRNA-lncRNA crosstalk in astrocytes and microglia to disarm neuroinflammatory triggers.Frontiers in molecular neuroscience · 2025Review
- Dementia and metabolic syndrome: a bibliometric analysis.Frontiers in aging neuroscience · 2024Article
- Extracellular and intracellular functions of coiled-coil domain containing 3.Journal of molecular cell biology · 2023Article
- Endothelial Cell Response in Kawasaki Disease and Multisystem Inflammatory Syndrome in Children.International journal of molecular sciences · 2023Article
- Shear stress leads to the dysfunction of endothelial cells through the Cav-1-mediated KLF2/eNOS/ERK signaling pathway under physiological conditions.Open life sciences · 2023Article
- Favine/CCDC3 deficiency accelerated atherosclerosis and thrombus formation is associated with decreased MEF2C-KLF2 pathway.iScience · 2022Article
- MOBT Alleviates Pulmonary Fibrosis through an lncITPF-hnRNP-l-Complex-Mediated Signaling Pathway.Molecules (Basel, Switzerland) · 2022Article
- MEF2C promotes M1 macrophage polarization and Th1 responses.Cellular & molecular immunology · 2022Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Endothelial cells play a major role in the initiation and perpetuation of the inflammatory process in health and disease, including their pivotal role in leukocyte recruitment. The role of pro-inflammatory transcription factors in this process has been well-described, including NF-κB. However, much less is known regarding transcription factors that play an anti-inflammatory role in endothelial cells. Myocyte enhancer factor 2 C (MEF2C) is a transcription factor known to regulate angiogenesis in endothelial cells. Here, we report that MEF2C plays a critical function as an inhibitor of endothelial cell inflammation. Tumor necrosis factor (TNF)-α inhibited MEF2C expression in endothelial cells. Knockdown of MEF2C in endothelial cells resulted in the upregulation of pro-inflammatory molecules and stimulated leukocyte adhesion to endothelial cells. MEF2C knockdown also resulted in NF-κB activation in endothelial cells. Conversely, MEF2C overexpression by adenovirus significantly repressed TNF-α induction of pro-inflammatory molecules, activation of NF-κB, and leukocyte adhesion to endothelial cells. This inhibition of leukocyte adhesion by MEF2C was partially mediated by induction of KLF2. In mice, lipopolysaccharide (LPS)-induced leukocyte adhesion to the retinal vasculature was significantly increased by endothelial cell-specific ablation of MEF2C. Taken together, these results demonstrate that MEF2C is a novel negative regulator of inflammation in endothelial cells and may represent a therapeutic target for vascular inflammation.
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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.