ArticleThe Journal of biological chemistry2011
Opposite regulation of the human apolipoprotein M gene by hepatocyte nuclear factor 1 and Jun transcription factors.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Apolipoprotein M: Structural insights, functional roles, and therapeutic approaches in vascular disease.The Journal of biological chemistry · 2026Review
- Identification and validation of efferocytosis-related biomarkers for the diagnosis of atherosclerosis based on bioinformatics and machine learning.European journal of medical research · 2025Article
- The role of novel adipokines in hepatocellular carcinoma progression: a mini review.American journal of cancer research · 2024Review
- Peroxisome Proliferator-Activated Receptor α in Lipoprotein Metabolism and Atherosclerotic Cardiovascular Disease.Biomedicines · 2023Review
- Plasma apolipoprotein M predicts overall survival in metastatic breast cancer patients.Breast cancer research and treatment · 2023Article
- The Opposite Effect of c-Jun Transcription Factor on Apolipoprotein E Gene Regulation in Hepatocytes and Macrophages.International journal of molecular sciences · 2019Article
- Effects of C2-Ceramide and Oltipraz on Hepatocyte Nuclear Factor-1 and Glutathione S-Transferase A1 in Acetaminophen-Mediated Acute Mice Liver Injury.Frontiers in pharmacology · 2018Article
- TGF-β Down-regulates Apolipoprotein M Expression through the TAK-1-JNK-c-Jun Pathway in HepG2 Cells.Lipids · 2017Article
- Global identification of the genetic networks and cis-regulatory elements of the cold response in zebrafish.Nucleic acids research · 2015Article
- Apolipoprotein M can discriminate HNF1A-MODY from Type 1 diabetes.Diabetic medicine : a journal of the British Diabetic Association · 2013Article
- Decreased plasma concentrations of apolipoprotein M in sepsis and systemic inflammatory response syndromes.Critical care (London, England) · 2012Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
HDL is a negative risk factor for atherosclerosis because of its multiple atheroprotective functions. Inflammation converts HDL particles from anti-atherogenic to pro-atherogenic, and this transformation is associated with changes in HDL structure and composition. Apolipoprotein M (apoM) has been recently shown to play a role in the maturation of HDL in plasma and to protect from atherosclerosis. ApoM gene is expressed primarily in the liver and kidney and is down-regulated by pro-inflammatory signals. We now show that the human apoM promoter harbors a dual specificity regulatory element in the proximal region that binds hepatocyte nuclear factor 1 (HNF-1) and members of the AP-1 family of pro-inflammatory transcription factors (c-Jun and JunB). Overexpression of c-Jun or JunB repressed both the basal and the HNF-1-mediated transactivation of the human apoM promoter. Treatment of HepG2 cells with potent inflammation-inducing phorbol esters or overexpression of PKCα was associated with a marked inhibition of apoM gene expression in a c-Jun/JunB-dependent manner. We provide evidence for a novel mechanism of inflammation-induced transcriptional repression that is based on the competition between HNF-1 and Jun proteins for binding to the same regulatory region. A similar mechanism accounts for the down-regulation of the liver-specific apolipoprotein A-II gene by Jun factors. Our studies provide novel insights on the mechanisms that control the expression of liver-specific apolipoprotein genes during inflammation and could affect the maturation and the functionality of HDL particles.
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