scholarly journals Oxidation induces a Cl − ‐dependent cation conductance in human red blood cells

2002 ◽  
Vol 539 (3) ◽  
pp. 847-855 ◽  
Author(s):  
Christophe Duranton ◽  
Stephan M. Huber ◽  
Florian Lang
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Human Red Blood Cells ◽  
Cation Conductance

scholarly journals Thrombospondin-1/CD47 signaling modulates transmembrane cation conductance, survival, and deformability of human red blood cells

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Rosi Bissinger ◽  
Polina Petkova-Kirova ◽  
Olga Mykhailova ◽  
Per-Arne Oldenborg ◽  
Elena Novikova ◽  
...  
Keyword(s):  
Cell Death ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Cell Types ◽  
Cell Interaction ◽  
Human Red Blood Cells ◽  
Cation Conductance ◽  
Thrombospondin 1 ◽  
Intracellular Ca ◽  
The Impact

Abstract Background Thrombospondin-1 (TSP-1), a Ca2+-binding trimeric glycoprotein secreted by multiple cell types, has been implicated in the pathophysiology of several clinical conditions. Signaling involving TSP-1, through its cognate receptor CD47, orchestrates a wide array of cellular functions including cytoskeletal organization, migration, cell-cell interaction, cell proliferation, autophagy, and apoptosis. In the present study, we investigated the impact of TSP-1/CD47 signaling on Ca2+ dynamics, survival, and deformability of human red blood cells (RBCs). Methods Whole-cell patch-clamp was employed to examine transmembrane cation conductance. RBC intracellular Ca2+ levels and multiple indices of RBC cell death were determined using cytofluorometry analysis. RBC morphology and microvesiculation were examined using imaging flow cytometry. RBC deformability was measured using laser-assisted optical rotational cell analyzer. Results Exposure of RBCs to recombinant human TSP-1 significantly increased RBC intracellular Ca2+ levels. As judged by electrophysiology experiments, TSP-1 treatment elicited an amiloride-sensitive inward current alluding to a possible Ca2+ influx via non-selective cation channels. Exogenous TSP-1 promoted microparticle shedding as well as enhancing Ca2+- and nitric oxide-mediated RBC cell death. Monoclonal (mouse IgG1) antibody-mediated CD47 ligation using 1F7 recapitulated the cell death-inducing effects of TSP-1. Furthermore, TSP-1 treatment altered RBC cell shape and stiffness (maximum elongation index). Conclusions Taken together, our data unravel a new role for TSP-1/CD47 signaling in mediating Ca2+ influx into RBCs, a mechanism potentially contributing to their dysfunction in a variety of systemic diseases.

scholarly journals Transbilayer distribution and mobility of phosphatidylinositol in human red blood cells.

1990 ◽  
Vol 265 (27) ◽  
pp. 16035-16038 ◽  
Author(s):  
P Bütikofer ◽  
Z W Lin ◽  
D T Chiu ◽  
B Lubin ◽  
F A Kuypers
Keyword(s):  
Red Blood Cells ◽  
Blood Cells ◽  
Human Red Blood Cells

scholarly journals Rhythmic glucose metabolism regulates the redox circadian clockwork in human red blood cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Ratnasekhar Ch ◽  
Guillaume Rey ◽  
Sandipan Ray ◽  
Pawan K. Jha ◽  
Paul C. Driscoll ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Red Blood Cells ◽  
Blood Cells ◽  
Mammalian Cells ◽  
Metabolic Flux ◽  
Pentose Phosphate ◽  
Human Red Blood Cells ◽  
Integral Process ◽  
Metabolic Oscillations ◽  
Human Rbcs

AbstractCircadian clocks coordinate mammalian behavior and physiology enabling organisms to anticipate 24-hour cycles. Transcription-translation feedback loops are thought to drive these clocks in most of mammalian cells. However, red blood cells (RBCs), which do not contain a nucleus, and cannot perform transcription or translation, nonetheless exhibit circadian redox rhythms. Here we show human RBCs display circadian regulation of glucose metabolism, which is required to sustain daily redox oscillations. We found daily rhythms of metabolite levels and flux through glycolysis and the pentose phosphate pathway (PPP). We show that inhibition of critical enzymes in either pathway abolished 24-hour rhythms in metabolic flux and redox oscillations, and determined that metabolic oscillations are necessary for redox rhythmicity. Furthermore, metabolic flux rhythms also occur in nucleated cells, and persist when the core transcriptional circadian clockwork is absent in Bmal1 knockouts. Thus, we propose that rhythmic glucose metabolism is an integral process in circadian rhythms.

scholarly journals Author Correction: Retention of Mitochondria in Mature Human Red Blood Cells as the Result of Autophagy Impairment in Rett Syndrome

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Diego Sbardella ◽  
Grazia Raffaella Tundo ◽  
Luisa Campagnolo ◽  
Giuseppe Valacchi ◽  
Augusto Orlandi ◽  
...  
Keyword(s):  
Red Blood Cells ◽  
Rett Syndrome ◽  
Blood Cells ◽  
Human Red Blood Cells

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