ArticlePflugers Archiv : European journal of physiology2013
Identification of the Ca²⁺ entry pathway involved in deoxygenation-induced phosphatidylserine exposure in red blood cells from patients with sickle cell disease.
Article in Pflugers Archiv : European journal of physiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
15 citing papers in PubMed, 25 citations in OpenAlex.
- Trial
- Microfluidic study of retention and elimination of abnormal red blood cells by human spleen with implications for sickle cell disease.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- The Role of RBC Oxidative Stress in Sickle Cell Disease: From the Molecular Basis to Pathologic Implications.Antioxidants (Basel, Switzerland) · 2021Review
- Cell and Gene Therapy for Anemia: Hematopoietic Stem Cells and Gene Editing.International journal of molecular sciences · 2021Review
- Pathophysiological Relevance of Renal Medullary Conditions on the Behaviour of Red Cells From Patients With Sickle Cell Anaemia.Frontiers in physiology · 2021Article
- Yoda1 and phosphatidylserine exposure in red cells from patients with sickle cell anaemia.Scientific reports · 2020Article
- The role of WNK in modulation of KCl cotransport activity in red cells from normal individuals and patients with sickle cell anaemia.Pflugers Archiv : European journal of physiology · 2019Article
- The Effect of Antioxidants on the Properties of Red Blood Cells From Patients With Sickle Cell Anemia.Frontiers in physiology · 2019Article
- Oxidative stress and phosphatidylserine exposure in red cells from patients with sickle cell anaemia.British journal of haematology · 2018Article
- Host genetics in malaria: lessons from mouse studies.Mammalian genome : official journal of the International Mammalian Genome Society · 2018Review
- The effect of xanthine oxidase and hypoxanthine on the permeability of red cells from patients with sickle cell anemia.Physiological reports · 2018Article
- Oxidative stress in β-thalassaemia and sickle cell disease.Redox biology · 2015Review
- Effects of 5-hydroxymethyl-2-furfural on the volume and membrane permeability of red blood cells from patients with sickle cell disease.The Journal of physiology · 2014Article
- Inhibitors of second messenger pathways and Ca(2+)-induced exposure of phosphatidylserine in red blood cells of patients with sickle cell disease.Pflugers Archiv : European journal of physiology · 2014Article
- Effects of o-vanillin on K⁺ transport of red blood cells from patients with sickle cell disease.Blood cells, molecules & diseasesArticle
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Phosphatidylserine (PS) exposure in red blood cells (RBCs) from sickle cell disease (SCD) patients is increased compared to levels in normal individuals and may participate in the anaemic and ischaemic complications of SCD. Exposure is increased by deoxygenation and occurs with elevation of intracellular Ca²⁺ to low micromolar levels. The Ca²⁺ entry step has not been defined but a role for the deoxygenation-induced pathway, Psickle, is postulated. Partial Psickle inhibitors 4-acetamido-4'-isothiocyanostilbene-2,2'-disulphonic acid (SITS), 4,4'-dithiocyano-2,2'-stilbene-disulphonic acid (DIDS) and dipyridamole inhibited deoxygenation-induced PS exposure (DIDS IC50, 118 nM). Inhibitors and activators of other pathways (including these stimulated by depolarisation, benzodiazepines, glutamate and stretch) were without effect. Zn²⁺ and Gd³⁺ stimulated PS exposure to high levels. In the case of Zn²⁺, this effect was independent of oxygen (and hence HbS polymerisation and RBC sickling) but required extracellular Ca²⁺. The effect was completely abolished when Zn²⁺ (100 μM) was added to RBCs suspended in autologous plasma, implying a requirement of high levels of free Zn²⁺.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
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.