ArticleInternational journal of molecular sciences2014
Characterization of timed changes in hepatic copper concentrations, methionine metabolism, gene expression, and global DNA methylation in the Jackson toxic milk mouse model of Wilson disease.
Article in International journal of molecular sciences, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 33 citations in OpenAlex.
- Experimental models of hepatic injury in Wilson disease: stage-specific mechanisms and translational applications.Frontiers in immunology · 2026Review
- N,N'-bis(2-mercaptoethyl)isophthalamide (NBMI) as a novel chelator for Wilson's disease.Free radical biology & medicine · 2025Article
- Copper homeostasis and pregnancy complications: a comprehensive review.Journal of assisted reproduction and genetics · 2025Review
- Effect of primary copper metabolism disturbance on elemental, protein, and lipid composition of the organs in Jackson toxic milk mouse.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2025Article
- Aberrant copper metabolism and hepatic inflammation cause neurological manifestations in a mouse model of Wilson's disease.Journal of neuroinflammation · 2024Article
- Transcriptomic evaluation of N6-methyladenosine modification can be used to identify differentially gene and immune-related biological processes in TX mice with liver fibrosis.Molecular biology reports · 2024Article
- Select Early-Life Environmental Exposures and DNA Methylation in the Placenta.Current environmental health reports · 2023Review
- Epigenetics in inflammatory liver diseases: A clinical perspective (Review).Experimental and therapeutic medicine · 2022Review
- Copper deposition in Wilson's disease causes male fertility decline by impairing reproductive hormone release through inducing apoptosis and inhibiting ERK signal in hypothalamic-pituitary of mice.Frontiers in endocrinology · 2022Article
- Copper associates with differential methylation in placentae from two US birth cohorts.Epigenetics · 2020Article
- Lipid and energy metabolism in Wilson disease.Liver research (Beijing, China) · 2020Article
- Dysregulated Choline, Methionine, and Aromatic Amino Acid Metabolism in Patients with Wilson Disease: Exploratory Metabolomic Profiling and Implications for Hepatic and Neurologic Phenotypes.International journal of molecular sciences · 2019Article
- Genetics and epigenetic factors of Wilson disease.Annals of translational medicine · 2019Review
- Reduced Neutrophil Extracellular Trap (NET) Formation During Systemic Inflammation in Mice With Menkes Disease and Wilson Disease: Copper Requirement for NET Release.Frontiers in immunology · 2019Article
- Wilson disease.Nature reviews. Disease primers · 2018Review
- Wilson disease: At the crossroads between genetics and epigenetics-A review of the evidence.Liver research (Beijing, China) · 2017Article
- Effects of Nonpurified and Choline Supplemented or Nonsupplemented Purified Diets on Hepatic Steatosis and Methionine Metabolism in C3H Mice.Metabolic syndrome and related disorders · 2016Article
- Wilson's disease: a comprehensive review of the molecular mechanisms.International journal of molecular sciences · 2015Review
Corrections and comments
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
Abstract
backgroundWilson disease (WD) is characterized by hepatic copper accumulation with progressive liver damage to cirrhosis. This study aimed to characterize the toxic milk mouse from The Jackson Laboratory (Bar Harbor, ME, USA) (tx-j) mouse model of WD according to changes over time in hepatic copper concentrations, methionine metabolism, global DNA methylation, and gene expression from gestational day 17 (fetal) to adulthood (28 weeks).
methodsIncluded liver histology and relevant biochemical analyses including hepatic copper quantification, S-adenosylmethionine (SAM) and S-adenosylhomocysteine (SAH) liver levels, qPCR for transcript levels of genes relevant to methionine metabolism and liver damage, and DNA dot blot for global DNA methylation.
resultsHepatic copper was lower in tx-j fetuses but higher in weanling (three weeks) and adult tx-j mice compared to controls. S-adenosylhomocysteinase transcript levels were significantly lower at all time points, except at three weeks, correlating negatively with copper levels and with consequent changes in the SAM:SAH methylation ratio and global DNA methylation.
conclusionCompared to controls, methionine metabolism including S-adenosylhomocysteinase gene expression is persistently different in the tx-j mice with consequent alterations in global DNA methylation in more advanced stages of liver disease. The inhibitory effect of copper accumulation on S-adenosylhomocysteinase expression is associated with progressively abnormal methionine metabolism and decreased methylation capacity and DNA global methylation.
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