ArticleThe Biochemical journal2006
Lectin-like oxidized low-density lipoprotein receptor-1 (LOX-1) transcriptional regulation by Oct-1 in human endothelial cells: implications for atherosclerosis.
Article in The Biochemical journal, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 73 citations in OpenAlex.
- The Role of NOX2-Derived Reactive Oxygen Species in the Induction of Endothelin-Converting Enzyme-1 by Angiotensin II.Antioxidants (Basel, Switzerland) · 2024Article
- LOX-1 mediates inflammatory activation of microglial cells through the p38-MAPK/NF-κB pathways under hypoxic-ischemic conditions.Cell communication and signaling : CCS · 2023Article
- Upregulation of Nogo-B by hypoxia inducible factor-1 and activator protein-1 in hepatocellular carcinoma.Cancer science · 2021Article
- APE1 inhibits foam cell formation from macrophages via LOX1 suppression.American journal of translational research · 2020Article
- Proteolytic Regulation of the Lectin-Like Oxidized Lipoprotein Receptor LOX-1.Frontiers in cardiovascular medicine · 2020Review
- Upregulated LOX-1 Receptor: Key Player of the Pathogenesis of Atherosclerosis.Current atherosclerosis reports · 2019Review
- Atherosclerosis: integration of its pathogenesis as a self-perpetuating propagating inflammation: a review.Cardiovascular endocrinology & metabolism · 2019Review
- OxHDL controls LOX-1 expression and plasma membrane localization through a mechanism dependent on NOX/ROS/NF-κB pathway on endothelial cells.Laboratory investigation; a journal of technical methods and pathology · 2019Article
- CKIP-1 limits foam cell formation and inhibits atherosclerosis by promoting degradation of Oct-1 by REGγ.Nature communications · 2019Article
- Article
- LOX-1 in atherosclerosis: biological functions and pharmacological modifiers.Cellular and molecular life sciences : CMLS · 2013Review
- LOX-1, OxLDL, and atherosclerosis.Mediators of inflammation · 2013Review
- Hyperlipidemia: a new therapeutic target for diabetic neuropathy.Journal of the peripheral nervous system : JPNS · 2009Review
- Curcumin eliminates oxidized LDL roles in activating hepatic stellate cells by suppressing gene expression of lectin-like oxidized LDL receptor-1.Laboratory investigation; a journal of technical methods and pathology · 2009Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LOX-1, a receptor for ox-LDL (oxidized low-density lipoprotein), has recently been determined to play a critical role in the progression of atherosclerosis. LOX-1 expression (mRNA and protein) has been shown to be up-regulated by pro-atherogenic stimuli, such as ox-LDL and Ang II (angiotensin II). However, the molecular mechanisms of these up-regulations are unclear. In the present study, we explored LOX-1 transcriptional promoter activation in response to ox-LDL and Ang II. Under basal states, LOX-1 core promoter (LOX-1 -35/+36) was found to be sufficient for its basal activity in HCAECs (human coronary artery endothelial cells). More importantly, we found that ox-LDL (60 microg/ml for 24 h) induced LOX-1 promoter activity significantly and that a 105 bp fragment (between nt -1599 and -1494) was required for this activation. Within this 106 bp fragment, there is a potential binding motif for the transcription factor Oct-1 (octamer-1). By electrophoretic mobility-shift assay, we observed the activation of Oct-1 by ox-LDL. The critical role of Oct-1 in ox-LDL-induced LOX-1 promoter activation was further confirmed by mutagenesis assay. For comparison, we also examined LOX-1 promoter activation in response to Ang II (1 micromol/l for 24 h). Interestingly, another promoter region, between nt -2336 and -1990, was required for Ang II-induced LOX-1 promoter activation. In conclusion, the present study strongly suggests that ox-LDL, by activating Oct-1, induces LOX-1 promoter activation. Furthermore, this study suggests that while ox-LDL and Ang II both induce LOX-1 expression in HCAECs, the underlying mechanisms of promoter activation are different from each other.
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