ArticleBritish journal of haematology2009
Ca2+-CaM activation of AMP deaminase contributes to adenine nucleotide dysregulation and phosphatidylserine externalization in human sickle erythrocytes.
Article in British journal of haematology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
- Multicenter, phase 1 study of etavopivat (FT-4202) treatment for up to 12 weeks in patients with sickle cell disease.Blood advances · 2024Trial
- Molecular and Immunometabolic Landscape of Erythrophagocytosis-induced Ferroptosis.Cardiovascular & hematological disorders drug targets · 2025Review
- A preliminary study of phosphodiesterases and adenylyl cyclase signaling pathway on red blood cell deformability of sickle cell patients.Frontiers in physiology · 2023Article
- Morphometric and Nanomechanical Features of Erythrocytes Characteristic of Early Pregnancy Loss.International journal of molecular sciences · 2022Article
- Dietary Selenium Deficiency Facilitated Reduced Stomatin and Phosphatidylserine Externalization, Increasing Erythrocyte Osmotic Fragility in Mice.Biological trace element research · 2021Article
- Acute Cycling Exercise Induces Changes in Red Blood Cell Deformability and Membrane Lipid Remodeling.International journal of molecular sciences · 2021Article
- Generation and Export of Red Blood Cell ATP in Health and Disease.Frontiers in physiology · 2021Review
- Ischemia-Reperfusion Injury in Sickle Cell Disease: From Basics to Therapeutics.The American journal of pathology · 2019Review
- Red Blood Cell Deformability, Vasoactive Mediators, and Adhesion.Frontiers in physiology · 2019Review
- Hypoxia modulates the purine salvage pathway and decreases red blood cell and supernatant levels of hypoxanthine during refrigerated storage.Haematologica · 2018Article
- Article
- Review
- Pathophisiology of sickle cell disease and new drugs for the treatment.Mediterranean journal of hematology and infectious diseases · 2009Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Ca2+-calmodulin (Ca2+-CaM) activates erythrocyte adenosine monophosphate deaminase (AMPD) in conditions of disturbed calcium homeostasis, prompting us to investigate adenine nucleotide metabolic dysregulation in sickle cell disease (SCD). However, higher ATP concentrations in reticulocytes, compared to erythrocytes, confound a comparative evaluation of SCD and normal RBCs. Therefore, a combination of centrifugation and antiCD71-labelled magnetic bead selection was used to prepare reticulocyte-poor fractions (reticulocytes <4% of total RBCs) of SCD RBCs. ATP and total adenine nucleotide concentrations were 12% lower in sickle erythrocytes compared to normal erythrocytes and inosine monophosphate (IMP) concentrations were threefold elevated (all P < 0.05). Furthermore, preincubation with a diffusible CaM antagonist slowed IMP accumulation in sickle erythrocytes during an experimental period of energy imbalance, thus showing that Ca2+-CaM activates AMPD in SCD. Finally, adenine treatment (100 micromol/l) of ex vivo SCD RBCs significantly expanded ATP levels (16% higher) and reduced phosphatidylserine (PS)-exposure, specifically those cells with the highest levels of PS externalization (46% fewer events) (both P-values <0.05 compared to untreated samples). We conclude that Ca2+-CaM activation of AMPD contributes to increased turnover of the adenine nucleotide pool in sickle erythrocytes and that this metabolic dysregulation promotes PS exposure that may contribute to the pathogenesis of SCD.
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