ArticleMolecular pharmacology2009
Mrp1 localization and function in cardiac mitochondria after doxorubicin.
Article in Molecular pharmacology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers, 1 of them a synthesis that pooled it.
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Who cites it
28 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Clinical and cost-effectiveness of pharmacogenomic testing for anthracycline-induced cardiotoxicity in childhood cancer: a systematic review and meta-analysis.Frontiers in pharmacology · 2025Pooled it
- Integrating Mendelian randomization and multi-omics analysis unravels gut microbiota-driven metabolic mechanisms in sepsis and identifies diagnostic biomarkers through experimental validation.APL bioengineering · 2026Article
- Decoding heart failure subtypes with neural networks via differential explanation analysis.Briefings in bioinformatics · 2025Article
- Cadmium transport by mammalian ATP-binding cassette transporters.Biometals : an international journal on the role of metal ions in biology, biochemistry, and medicine · 2024Review
- Potential roles of 4HNE-adducted protein in serum extracellular vesicles as an early indicator of oxidative response against doxorubicin-induced cardiomyopathy in rats.Current research in toxicology · 2023Article
- Genetics of Anthracycline-Associated Cardiotoxicity.Frontiers in cardiovascular medicine · 2022Review
- Genetic Susceptibility and Mechanisms Underlying the Pathogenesis of Anthracycline-Associated Cardiotoxicity.Oxidative medicine and cellular longevity · 2022Review
- Review
- In vitro function and in situ localization of Multidrug Resistance-associated Protein (MRP)1 (ABCC1) suggest a protective role against methyl mercury-induced oxidative stress in the human placenta.Archives of toxicology · 2020Article
- Drug-drug-gene interactions and adverse drug reactions.The pharmacogenomics journal · 2020Review
- Linker Domains: Why ABC Transporters 'Live in Fragments no Longer'.Trends in biochemical sciences · 2020Review
- Plausible biochemical mechanisms of chemotherapy-induced cognitive impairment ("chemobrain"), a condition that significantly impairs the quality of life of many cancer survivors.Biochimica et biophysica acta. Molecular basis of disease · 2019Review
- Pediatric Anthracycline-Induced Cardiotoxicity: Mechanisms, Pharmacogenomics, and Pluripotent Stem-Cell Modeling.Clinical pharmacology and therapeutics · 2019Review
- Delivery of siRNA in vitro and in vivo using PEI-capped porous silicon nanoparticles to silence MRP1 and inhibit proliferation in glioblastoma.Journal of nanobiotechnology · 2018Article
- Sulforaphane protects the heart from doxorubicin-induced toxicity.Free radical biology & medicine · 2015Article
- Mitochondria of a human multidrug-resistant hepatocellular carcinoma cell line constitutively express inducible nitric oxide synthase in the inner membrane.Journal of cellular and molecular medicine · 2015Article
- Article
- The 2013 SFRBM discovery award: selected discoveries from the butterfield laboratory of oxidative stress and its sequela in brain in cognitive disorders exemplified by Alzheimer disease and chemotherapy induced cognitive impairment.Free radical biology & medicine · 2014Review
- Quantitative proteomics analysis identifies mitochondria as therapeutic targets of multidrug-resistance in ovarian cancer.Theranostics · 2014Article
- Protection from oxidative and electrophilic stress in the Gsta4-null mouse heart.Cardiovascular toxicology · 2013Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Multidrug resistance-associated protein 1 (Mrp1; Abcc1) is expressed in sarcolemma of murine heart, where it probably protects the cardiomyocyte by mediating efflux of endo- and xenobiotics. We used doxorubicin (DOX), a chemotherapeutic drug known to induce oxidative stress and thereby cardiac injury, as a model cardiotoxic compound and observed changes in the Mrp1 expression pattern in cardiac tissue of DOX-versus saline-treated mice. Confocal immunofluorescent and immunogold electron microscopy, together with subcellular fractionation followed by immunoblot analyses and transport measurements, localized functional Mrp1 to mitochondria after DOX. Expressions of Mrp1 in heart homogenate, sarcolemma, and submitochondrial particles (SMP) were increased 1.6-, 2-, and 3-fold, respectively, at 24 h after DOX. Mitochondrial Mrp1 expression was markedly increased 72 h after DOX, whereas transport of Mrp1 substrates in SMP was maximal at 24 h. ATP-dependent transport in SMP occurred into an osmotically sensitive space and was inhibited by the anti-MRP1 antibody QCRL3. Adduction of a 190-kDa protein with the reactive lipid peroxidation product 4-hydroxy-2-nonenal (HNE) was detected in SMP and was maximal at 72 h after DOX; immunoprecipitation confirmed Mrp1-HNE adduction. In vitro, HNE (10 muM) inhibited mitochondrial respiration and transport activity in SMP, suggesting that Mrp1 is adversely affected by oxidative stress. These data demonstrate that after DOX, functional Mrp1 is detected in mitochondria in addition to that in sarcolemma; however, adduction with HNE inhibits Mrp1 activity. Mrp1 may serve to protect the heart by mediating the efflux of toxic products of oxidative stress from mitochondria and cardiomyocytes.
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