ArticleThe Biochemical journal2007
Oxidative stress regulates IGF1R expression in vascular smooth-muscle cells via p53 and HDAC recruitment.
Article in The Biochemical journal, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 50 citations in OpenAlex.
- Vascular Smooth Muscle Cells: A Therapeutic Target in Atherosclerosis.Reviews in cardiovascular medicine · 2025Review
- Genome-Wide Acetylation Modification of H3K27ac in Bovine Rumen Cell Following Butyrate Exposure.Biomolecules · 2023Article
- The role of p53 in the alternation of vascular functions.Frontiers in pharmacology · 2022Review
- Inducing Energetic Switching Using Klotho Improves Vascular Smooth Muscle Cell Phenotype.International journal of molecular sciences · 2021Article
- New Insights for BPIFB4 in Cardiovascular Therapy.International journal of molecular sciences · 2020Review
- Developmental programming: Prenatal bisphenol A treatment disrupts mediators of placental function in sheep.Chemosphere · 2020Article
- Article
- NADPH oxidases: key modulators in aging and age-related cardiovascular diseases?Clinical science (London, England : 1979) · 2016Review
- Classification of Promoters Based on the Combination of Core Promoter Elements Exhibits Different Histone Modification Patterns.PloS one · 2016Article
- Epigenetic reprogramming in atherosclerosis.Current atherosclerosis reports · 2015Review
- Article
- The transcription factor p53: not a repressor, solely an activator.Cell cycle (Georgetown, Tex.) · 2014Article
- Epigenetic regulation of vascular smooth muscle cell function in atherosclerosis.Current atherosclerosis reports · 2013Review
- Advanced glycation end products promote human aortic smooth muscle cell calcification in vitro via activating NF-κB and down-regulating IGF1R expression.Acta pharmacologica Sinica · 2013Article
- Upregulation of the E3 ligase NEDD4-1 by oxidative stress degrades IGF-1 receptor protein in neurodegeneration.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- The p53 network: cellular and systemic DNA damage responses in aging and cancer.Trends in genetics : TIG · 2012Review
- Article
- Insulin-like growth factor-I regulation of immune function: a potential therapeutic target in autoimmune diseases?Pharmacological reviews · 2010Review
- Do non-targeted effects increase or decrease low dose risk in relation to the linear-non-threshold (LNT) model?Mutation research · 2010Review
- Atherogenic factors and their epigenetic relationships.International journal of vascular medicine · 2010Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Apoptosis of VSMCs (vascular smooth-muscle cells) leads to features of atherosclerotic plaque instability. We have demonstrated previously that plaque-derived VSMCs have reduced IGF1 (insulin-like growth factor 1) signalling, resulting from a decrease in the expression of IGF1R (IGF1 receptor) compared with normal aortic VSMCs [Patel, Zhang, Siddle, Soos, Goddard, Weissberg and Bennett (2001) Circ. Res. 88, 895-902]. In the present study, we show that apoptosis induced by oxidative stress is inhibited by ectopic expression of IGF1R. Oxidative stress repressed IGF1R expression at multiple levels, and this was also blocked by mutant p53. Oxidative stress also induced p53 phosphorylation and apoptosis in VSMCs. p53 negatively regulated IGF1R promoter activity and expression and, consistent with this, p53-/- VSMCs demonstrated increased IGF1R expression, both in vitro and in advanced atherosclerotic plaques in vivo. Oxidative-stress-induced interaction of endogenous p53 with TBP (TATA-box-binding protein) was dependent on p53 phosphorylation. Oxidative stress also increased the association of p53 with HDAC1 (histone deacetylase 1). Trichostatin A, a specific HDAC inhibitor, or p300 overexpression relieved the repression of IGF1R following oxidative stress. Furthermore, acetylated histone-4 association with the IGF1R promoter was reduced in cells subjected to oxidative stress. These results suggest that oxidative-stress-induced repression of IGF1R is mediated by the association of phosphorylated p53 with the IGF1R promoter via TBP, and by the subsequent recruitment of chromatin-modifying proteins, such as HDAC1, to the IGF1R promoter-TBP-p53 complex.
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Registered trials
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.