ArticlePflugers Archiv : European journal of physiology2009
Disruption of the Gardos channel (KCa3.1) in mice causes subtle erythrocyte macrocytosis and progressive splenomegaly.
Article in Pflugers Archiv : European journal of physiology, 2009. 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.
- Innate Variability in Physiological and Omics Aspects of the Beta Thalassemia Trait-Specific Donor Variation Effects.Frontiers in physiology · 2022Article
- Article
- Review
- Pharmacology of Small- and Intermediate-Conductance Calcium-Activated Potassium Channels.Annual review of pharmacology and toxicology · 2020Review
- Article
- Combined genetic disruption of K-Cl cotransporters and Gardos channel KCNN4 rescues erythrocyte dehydration in the SAD mouse model of sickle cell disease.Blood cells, molecules & diseases · 2019Article
- KCa3.1 Transgene Induction in Murine Intestinal Epithelium Causes Duodenal Chyme Accumulation and Impairs Duodenal Contractility.International journal of molecular sciences · 2019Article
- The calcium-activated potassium channel KCa3.1 is an important modulator of hepatic injury.Scientific reports · 2016Article
- The calcium-activated potassium channel KCa3.1 plays a central role in the chemotactic response of mammalian neutrophils.Acta physiologica (Oxford, England) · 2016Article
- Genetic deficit of KBritish journal of pharmacology · 2015Article
- An alternative to force.eLife · 2015Article
- Article
- Modulation of K(Ca)3.1 channels by eicosanoids, omega-3 fatty acids, and molecular determinants.PloS one · 2014Article
- Role of the K(Ca)3.1 K+ channel in auricular lymph node CD4+ T-lymphocyte function of the delayed-type hypersensitivity model.British journal of pharmacology · 2013Article
- Novel phenolic inhibitors of small/intermediate-conductance Ca²⁺-activated K⁺ channels, KCa3.1 and KCa2.3.PloS one · 2013Article
- Genetic KCa3.1-deficiency produces locomotor hyperactivity and alterations in cerebral monoamine levels.PloS one · 2012Article
- Microglial KCa3.1 Channels as a Potential Therapeutic Target for Alzheimer's Disease.International journal of Alzheimer's disease · 2012Article
- Trpc2 depletion protects red blood cells from oxidative stress-induced hemolysis.Experimental hematology · 2012Article
- Functional KCa3.1 K+ channels are required for human fibrocyte migration.The Journal of allergy and clinical immunology · 2011Article
- The Lymphocyte Potassium Channels Kv1.3 and KCa3.1 as Targets for Immunosuppression.Drug development research · 2011Article
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10 authors.
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Abstract
Gardos channel, the erythrocyte Ca(2+)-activated K(+) channel (K(Ca)3.1), is considered a major regulator of red blood cell (RBC) volume by mediating efflux of potassium and thus cell dehydration and shrinkage. However, the functional importance of K(Ca)3.1 in RBC in vivo is incompletely understood. Here, we used K(Ca)3.1(-/-)-mice to investigate the consequences of K(Ca)3.1 deficiency for RBC indices, functions, and sequestration. RBCs of K(Ca)3.1(-/-)-mice of all ages were mildly macrocytic but their biconcave appearance being preserved. RBC number, total hemoglobin, and hematocrit were unchanged in the adult K(Ca)3.1(-/-)-mice and increased in the premature K(Ca)3.1(-/-)-mice. Filterability, Ca(2+)-dependent volume decrease and osmotic tolerance of RBCs lacking K(Ca)3.1 were noticeably reduced when compared to RBC of wild-type littermates. Deformability to increasing shear stress was unchanged. Strikingly, K(Ca)3.1(-/-)-mice developed progressive splenomegaly which was considerable ( approximately 200% of controls) in the >6-month-old mice and was paralleled by increased iron deposition in the aged mice presumably as a consequence of enhanced RBC sequestration. Daily injections of the K(Ca)3.1-blocker TRAM-34 (120 mg/kg) also produced mild splenomegaly in wild-type mice. We conclude that genetic deficit of erythroid K(Ca)3.1 causes mild RBC macrocytosis, presumably leading to reduced filterability, and impairs volume regulation. These RBC defects result in mild but progressive splenomegaly.
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