ArticleAntioxidants & redox signaling2015
The Interplay Between Peroxiredoxin-2 and Nuclear Factor-Erythroid 2 Is Important in Limiting Oxidative Mediated Dysfunction in β-Thalassemic Erythropoiesis.
Article in Antioxidants & redox signaling, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 52 citations in OpenAlex.
- Mitapivat metabolically reprograms human β-thalassemic erythroblasts, increasing their responsiveness to oxidation.Blood advances · 2025Article
- Modulation of Antioxidant Enzyme Expression of In Vitro Culture-Derived Reticulocytes.Antioxidants (Basel, Switzerland) · 2024Article
- Nrf2 Plays a Key Role in Erythropoiesis during Aging.Antioxidants (Basel, Switzerland) · 2024Article
- Exploring the bone marrow micro environment in thalassemia patients: potential therapeutic alternatives.Frontiers in immunology · 2024Review
- Elevated CDKN1A (P21) mediates β-thalassemia erythroid apoptosis, but its loss does not improve β-thalassemic erythropoiesis.Blood advances · 2023Article
- Duality of Nrf2 in iron-overload cardiomyopathy.Haematologica · 2023Article
- In Humanized Sickle Cell Mice, Imatinib Protects Against Sickle Cell-Related Injury.HemaSphere · 2023Article
- Discovery-Based Proteomics Identify Skeletal Muscle Mitochondrial Alterations as an Early Metabolic Defect in a Mouse Model of β-Thalassemia.International journal of molecular sciences · 2023Article
- Pharmacological Induction of Fetal Hemoglobin in β-Thalassemia and Sickle Cell Disease: An Updated Perspective.Pharmaceuticals (Basel, Switzerland) · 2022Review
- Redox Balance in β-Thalassemia and Sickle Cell Disease: A Love and Hate Relationship.Antioxidants (Basel, Switzerland) · 2022Review
- Adaptative Up-Regulation of PRX2 and PRX5 Expression Characterizes Brain from a Mouse Model of Chorea-Acanthocytosis.Antioxidants (Basel, Switzerland) · 2021Article
- The pyruvate kinase activator mitapivat reduces hemolysis and improves anemia in a β-thalassemia mouse model.The Journal of clinical investigation · 2021Article
- Active hematopoiesis triggers exosomal release of PRDX2 that promotes osteoclast formation.Physiological reports · 2021Article
- Oxidation Impacts the Intracellular Signaling Machinery in Hematological Disorders.Antioxidants (Basel, Switzerland) · 2020Review
- Knockout Mouse Models for Peroxiredoxins.Antioxidants (Basel, Switzerland) · 2020Review
- Bitopertin, a selective oral GLYT1 inhibitor, improves anemia in a mouse model of β-thalassemia.JCI insight · 2019Article
- Plasma peroxiredoxin changes and inflammatory cytokines support the involvement of neuro-inflammation and oxidative stress in Autism Spectrum Disorder.Journal of translational medicine · 2019Article
- Effects of KEAP1 Silencing on the Regulation of NRF2 Activity in Neuroendocrine Lung Tumors.International journal of molecular sciences · 2019Article
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Authors and funding
12 authors at 5 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimsβ-Thalassemia is a common inherited red cell disorder characterized by ineffective erythropoiesis and severe oxidative stress. Peroxiredoxin-2 (Prx2), a typical 2-cysteine peroxiredoxin, is upregulated during β-thalassemic erythropoiesis, but its contribution to stress erythropoiesis, a common feature of thalassemia, is yet to be fully defined.
resultsHere, we showed that Prx2(-/-) mice displayed reactive oxygen species related abnormalities in erythropoiesis similar to that of Hbb(th3/+) mice associated with activation of redox response transcriptional factor nuclear factor-erythroid 2 (Nrf2). We generated β-thalassemic mice genetically lacking Prx2 (Prx2(-/-)Hbb(th3/+)) and documented a worsened β-thalassemic hematological phenotype with severe ineffective erythropoiesis. To further validate a key role of Prx2 in stress erythropoiesis, we administrated fused recombinant PEP1Prx2 to Hbb(th3/+) mice and documented a decrease in ineffective erythropoiesis. We further show that Prx2 effects are mediated by activation of Nrf2 and upregulation of genes that protect against oxidative damage such as gluthatione S-transferase, heme-oxygenase-1, and NADPH dehydrogenase quinone-1. INNOVATION: We propose Prx2 as a key antioxidant system and Nrf2 activation is a cellular adaptive process in response to oxidative stress, resulting in upregulation of antioxidant (antioxidant responsive element) genes required to ensure cell survival.
conclusionOur data shed new light on adaptive mechanisms against oxidative damage through the interplay of Prx2 and Nrf2 during stress erythropoiesis and suggest new therapeutic options to decrease ineffective erythropoiesis by modulation of endogenous antioxidant systems.
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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.