Adhesion of klotho‐deficient eryptotic erythrocytes to endothelial cells

Abed, Majed; Towhid, Syeda Tasneem; Feger, Martina; Schmidt, Sebastian; Kuro‐o, Makoto; Gawaz, Meinrad; Läng, Florian

doi:10.1111/apha.12046

Cited by 59 publications

(93 citation statements)

References 93 publications

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“…An example of this is thromboxane, which was found to stimulate RBCs by inducing PS exposure on their surfaces, followed by an increase in cytosolic calcium content [76]. These responses have been found to be associated with reduced membrane deformability, increased adhesion, formation of pathomorphologies and a precursor to eryptosis [91][92][93]. The PS exposure further increases the adherence of RBCs to platelets and induces thrombosis [93].…”

Section: Rbc and Platelet Interactions In Ramentioning

confidence: 99%

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Olumuyiwa-Akeredolu

Pretorius

2015

Rheumatol Int

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Section: Rbc and Platelet Interactions In Ramentioning

confidence: 99%

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Olumuyiwa-Akeredolu

Pretorius

2015

Rheumatol Int

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“…Moreover, phosphatdylserine exposing erythrocytes may adhere to the vascular wall [77] and stimulate clotting as well as thrombosis [78][79][80]. Accordingly, excessive eryptosis may interfere with microcirculation [32,78,[81][82][83][84].…”

Section: Discussionmentioning

confidence: 99%

“…Eryptosis is further stimulated by ceramide [32], oxidative stress [30], energy depletion [30], activated caspases [30,33,34], casein kinase 1α, Janus-activated kinase JAK3, protein kinase C and p38 kinase [30]. Eryptosis is inhibited by AMP activated kinase AMPK, cGMP-dependent protein kinase, PAK2 kinase, and sorafenib/sunitinib sensitive kinases [30].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Suicidal Erythrocyte Death by Garcinol

Fazio

Briglia

Faggio

et al. 2015

Cell Physiol Biochem

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Background/Aims: The benzophenone garcinol from dried fruit rind of Garcinia indica counteracts malignancy, an effect at least in part due to stimulation of apoptosis. The proapototic effect of garcinol is attributed in part to inhibition of histone acetyltransferases and thus modification of gene expression. Moreover, garcinol triggers mitochondrial depolarisation. Erythrocytes lack gene expression and mitochondria but are nevertheless able to enter apoptosis-like suicidal death or eryptosis, which is characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Stimulators of eryptosis include oxidative stress, energy depletion and Ca 2+ entry with increase of cytosolic Ca 2+ activity ([Ca 2+ ] i ). The present study explored, whether and how garcinol induces eryptosis. Methods: To this end, phosphatidylserine exposure at the cell surface was estimated from annexin-V-binding, cell volume from forward scatter, hemolysis from hemoglobin release, [Ca 2+ ] i from Fluo3-fluorescence, ROS formation from DCFDA dependent fluorescence and cytosolic ATP levels utilizing a luciferin-luciferase-based assay. Results: A 24 hours exposure of human erythrocytes to garcinol (2.5 or 5 µM) significantly increased the percentage of annexin-V-binding cells. Garcinol decreased (at 1 µM and 2.5 µM) or increased (at 5 µM) forward scatter. Garcinol (5 µM) further increased Fluo3-fluorescence, increased DCFDA fluorescence, and decreased cytosolic ATP levels. The effect of garcinol on annexin-V-binding was significantly blunted, but not abolished by removal of extracellular Ca 2+ . Conclusions: Garcinol triggers cell shrinkage and phospholipid scrambling of the erythrocyte cell membrane, an effect in part due to stimulation of ROS formation, energy depletion and Ca 2+ entry.

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“…Hallmarks of eryptosis are cell shrinkage [61] and cell membrane scrambling with phosphatidylserine translocation to the cell surface [58]. Cellular mechanisms participating in the orchestration of eryptosis include increase of cytosolic Ca 2+ activity ([Ca 2+ ] i ) [58], ceramide [62], caspases [58,63,64], G-protein Galphai2 [65], casein kinase 1α [58], Janus-activated kinase JAK3 [58], protein kinase C [58], and p38 kinase [58]. Eryptosis is suppressed by AMP activated kinase AMPK [58], cGMP-dependent protein kinase [58], mitogen and stress activated kinase MSK1/2 [66], PAK2 kinase [58] and sorafenib/sunitinib sensitive kinases [58].…”

Section: Introductionmentioning

confidence: 99%

Stimulation of Eryptosis by Afatinib

Bhuyan

Läng

2018

Cell Physiol Biochem

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Background/Aims: The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor afatinib is primarily utilized for the treatment of non-small cell lung carcinoma. The drug is at least partially effective by triggering suicidal tumor cell death. Side effects of afatinib treatment include anemia. At least in theory, afatinib induced anemia could be secondary to stimulation of suicidal erythrocyte death or eryptosis, characterized by cell shrinkage and cell membrane scrambling with phosphatidylserine translocation to the erythrocyte surface. Signaling potentially stimulating eryptosis include increase of cytosolic Ca 2+ activity ([Ca 2+ ] i ), induction of oxidative stress, and increase of ceramide abundance. The present study explored, whether afatinib induces eryptosis and, if so, whether its effect involves Ca 2+ entry, oxidative stress, and/or ceramide. Methods: Flow cytometry was employed to quantify phosphatidylserine exposure at the cell surface from annexin-V-binding, cell volume from forward scatter, [Ca 2+ ] i from Fluo3-fluorescence, reactive oxygen species (ROS) abundance from DCFDA dependent fluorescence, and ceramide abundance utilizing specific antibodies. Results: A 48 hours exposure of human erythrocytes to afatinib (≥ 4 µg/ml) significantly increased the percentage of annexin-V-binding cells and significantly decreased forward scatter. Afatinib significantly increased Fluo3-fluorescence, DCFDA fluorescence and ceramide abundance. The effect of afatinib on annexin-V-binding and forward scatter was significantly blunted by removal of extracellular Ca 2+ . Conclusions: Afatinib triggers phospholipid scrambling of the erythrocyte cell membrane, an effect at least in part due to Ca 2+ entry, oxidative stress, and ceramide.

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Adhesion of klotho‐deficient eryptotic erythrocytes to endothelial cells

Abstract: klotho(-/-) erythrocytes are particularly sensitive to osmotic shock, and enhanced eryptosis of klotho(-/-) erythrocytes is paralleled by enhanced adhesion to endothelial CXCL16.

Cited by 59 publications

References 93 publications

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Platelet and red blood cell interactions and their role in rheumatoid arthritis

Stimulation of Suicidal Erythrocyte Death by Garcinol

Stimulation of Eryptosis by Afatinib

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