ArticleCells2020
Red Blood Cell Peroxynitrite Causes Endothelial Dysfunction in Type 2 Diabetes Mellitus via Arginase.
Article in Cells, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 56 citations in OpenAlex.
- Insulin facilitates entry of calcium ions into human and murine erythrocytes via Piezo1: a newly identified mechanism with implications for type 2 diabetes.The FEBS journal · 2025Article
- Endothelial Dysfunction: Redox Imbalance, NLRP3 Inflammasome, and Inflammatory Responses in Cardiovascular Diseases.Antioxidants (Basel, Switzerland) · 2025Review
- Biochemistry, pharmacology, and in vivo function of arginases.Pharmacological reviews · 2025Review
- EndothelialCurrent diabetes reviews · 2025Review
- Review
- Role of Peroxynitrite in the Pathogenesis of Parkinson's Disease and Its Fluorescence Imaging-Based Detection.Biosensors · 2024Review
- New Insights into Endothelial Dysfunction in Cardiometabolic Diseases: Potential Mechanisms and Clinical Implications.International journal of molecular sciences · 2024Review
- Mitochondrial Dysfunction in Endothelial Progenitor Cells: Unraveling Insights from Vascular Endothelial Cells.Biology · 2024Review
- Recent Progress of Spectroscopic Probes for Peroxynitrite and Their Potential Medical Diagnostic Applications.International journal of molecular sciences · 2023Review
- Pathophysiology of Red Blood Cell Dysfunction in Diabetes and Its Complications.Pathophysiology : the official journal of the International Society for Pathophysiology · 2023Review
- Vascular nitric oxide resistance in type 2 diabetes.Cell death & disease · 2023Review
- Molecular Study on Twin Cohort with Discordant Birth Weight.Antioxidants (Basel, Switzerland) · 2023Article
- Unexplored Roles of Erythrocytes in Atherothrombotic Stroke.Neurology international · 2023Review
- Mechanism of the antidiabetic action ofFrontiers in nutrition · 2023Review
- Molecular Background of Toxic-Substances-Induced Morphological Alterations in the Umbilical Cord Vessels and Fetal Red Blood Cells.International journal of molecular sciences · 2022Article
- Effect of Obstructive Sleep Apnea and CPAP Treatment on the Bioavailability of Erythrocyte and Plasma Nitric Oxide.International journal of environmental research and public health · 2022Article
- Arginase: shedding light on the mechanisms and opportunities in cardiovascular diseases.Cell death discovery · 2022Review
- Role of Erythrocytes in Nitric Oxide Metabolism and Paracrine Regulation of Endothelial Function.Antioxidants (Basel, Switzerland) · 2022Review
- Red Cell Distribution Width Is Independently Associated with Mortality in Sepsis.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2022Article
- Low grade intravascular hemolysis associates with peripheral nerve injury in type 2 diabetes.PloS one · 2022Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
We recently showed that red blood cells (RBCs) from patients with type 2 diabetes mellitus (T2DM-RBCs) induce endothelial dysfunction through a mechanism involving arginase I and reactive oxygen species. Peroxynitrite is known to activate arginase in endothelial cells. Whether peroxynitrite regulates arginase activity in RBCs, and whether it is involved in the cross-talk between RBCs and the vasculature in T2DM, is unclear and elusive. The present study was designed to test the hypothesis that endothelial dysfunction induced by T2DM-RBCs is driven by peroxynitrite and upregulation of arginase. RBCs were isolated from patients with T2DM and healthy age matched controls. RBCs were co-incubated with aortae isolated from wild type rats for 18 h in the absence and presence of peroxynitrite scavenger FeTTPS. Evaluation of endothelial function in organ chambers by cumulative addition of acetylcholine as well as measurement of RBC and vessel arginase activity was performed. In another set of experiments, RBCs isolated from healthy subjects (Healthy RBCs) were incubated with the peroxynitrite donor SIN-1 with subsequent evaluation of endothelial function and arginase activity. T2DM-RBCs, but not Healthy RBCs, induced impairment in endothelial function, which was fully reversed by scavenging of RBC but not vascular peroxynitrite with FeTPPS. Arginase activity was up-regulated by the peroxynitrite donor SIN-1 in Healthy RBCs, an effect that was inhibited by FeTTPS. Healthy RBCs co-incubated with aortae in the presence of SIN-1 caused impairment of endothelial function, which was inhibited by FeTTPS or the arginase inhibitor ABH. T2DM-RBCs induced up-regulation of vascular arginase, an effect that was fully inhibited by FeTTPS. Collectively, our data indicate that RBCs impair endothelial function in T2DM via an effect that is driven by a peroxynitrite-mediated increase in arginase activity. This mechanism may be targeted in patients with T2DM for improvement in endothelial function.
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