Triggering of Programmed Erythrocyte Death by Alantolactone

Alzoubi, Kousi; Calabrò, Salvatrice; Egler, Jasmin; Faggio, Caterina; Läng, Florian

doi:10.3390/toxins6123596

Cited by 7 publications

(3 citation statements)

References 97 publications

(114 reference statements)

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“…During cell injury, apoptosis, or activation, PS is externalized to the outer membrane and accompanied with vesicles release, also called microparticles (MPs), which expose PS and express membrane antigens on their surfaces [ 8 , 9 ]. Moreover, under the stimulation of anticarcinogenic drugs such as PRIMA-1 and alantolactone et al , RBC may enter suicidal death or eryptosis, which is characterized by cell shrinkage and cell membrane scrambling with PS exposure at the RBC surface [ 10 , 11 ]. PS is necessary for assembly of tenase and prothrombinase that results in thrombin generation [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Indolic Uremic Solutes Enhance Procoagulant Activity of Red Blood Cells through Phosphatidylserine Exposure and Microparticle Release

Gao

Dong

et al. 2015

Toxins

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Increased accumulation of indolic uremic solutes in the blood of uremic patients contributes to the risk of thrombotic events. Red blood cells (RBCs), the most abundant blood cells in circulation, may be a privileged target of these solutes. However, the effect of uremic solutes indoxyl sulfate (IS) and indole-3-acetic acid (IAA) on procoagulant activity (PCA) of erythrocyte is unclear. Here, RBCs from healthy adults were treated with IS and IAA (mean and maximal concentrations reported in uremic patients). Phosphatidylserine (PS) exposure of RBCs and their microparticles (MPs) release were labeled with Alexa Fluor 488-lactadherin and detected by flow cytometer. Cytosolic Ca2+ ([Ca2+]) with Fluo 3/AM was analyzed by flow cytometer. PCA was assessed by clotting time and purified coagulation complex assays. We found that PS exposure, MPs generation, and consequent PCA of RBCs at mean concentrations of IS and IAA enhanced and peaked in maximal uremic concentrations. Moreover, 128 nM lactadherin, a PS inhibitor, inhibited over 90% PCA of RBCs and RMPs. Eryptosis or damage, by indolic uremic solutes was due to, at least partially, the increase of cytosolic [Ca2+]. Our results suggest that RBC eryptosis in uremic solutes IS and IAA plays an important role in thrombus formation through releasing RMPs and exposing PS. Lactadherin acts as an efficient anticoagulant in this process.

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Section: Introductionmentioning

confidence: 99%

Indolic Uremic Solutes Enhance Procoagulant Activity of Red Blood Cells through Phosphatidylserine Exposure and Microparticle Release

Gao

Dong

et al. 2015

Toxins

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“…Ionomycin, a calcium ionophore, has been widely used to induce eryptosis in erythrocytes 12,17,18,19,20,21,22,23,24,25,26 . Ionomycin has both hydrophilic and hydrophobic groups, which are necessary to bind and capture Ca 2+ ion, and transport it to the cytosolic space 27,28,29 .…”

Section: Introductionmentioning

confidence: 99%

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Bigdelou

Farnoud

2020

JoVE

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Eryptosis, erythrocyte programmed cell death, occurs in a number of hematological diseases and during injury to erythrocytes. A hallmark of eryptotic cells is the loss of compositional asymmetry of the cell membrane, leading to the translocation of phosphatidylserine to the membrane outer leaflet. This process is triggered by increased intracellular concentration of Ca 2+ , which activates scramblase, an enzyme that facilitates bidirectional movement of phospholipids between membrane leaflets. Given the importance of eryptosis in various diseased conditions, there have been efforts to induce eryptosis in vitro. Such efforts have generally relied on the calcium ionophore, ionomycin, to enhance intracellular Ca 2+ concentration and induce eryptosis. However, many discrepancies have been reported in the literature regarding the procedure for inducing eryptosis using ionomycin. Herein, we report a step-by-step protocol for ionomycin-induced eryptosis in human erythrocytes. We focus on important steps in the procedure including the ionophore concentration, incubation time, and glucose depletion, and provide representative result. This protocol can be used to reproducibly induce eryptosis in the laboratory.

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“…Eryptosis, the suicidal death of erythrocytes, is caused by several anemia-inducing endogenous substances, diabetes, chronic renal failure, hemolytic uremic syndrome, sepsis, malaria, iron deficiency, and exogenous substances [22]. Several drugs have been described to trigger eryptosis, like alantolactone, gramicidin, naphthazarin, nelfinavir, hemolysin, listeriolysin, paclitaxel, chlorpromazine, cyclosporine, methylglyoxal, amyloid peptides, anandamide, Bay-5884, curcumin, valinomycin, aluminium, mercury, lead, and copper [22][23][24][25][26]. Eryptosis is characterized by phosphatidylserine exposure at the erythrocyte surface [27].…”

Section: Introductionmentioning

confidence: 99%

Effect of Lipophilic Bismuth Nanoparticles on Erythrocytes

Hernandez-Delgadillo

Badireddy

Zaragoza-Magaña

et al. 2015

Journal of Nanomaterials

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Lipophilic bismuth dimercaptopropanol nanoparticles (BisBAL NPs) have a very important antimicrobial activity; however their effect on human cells or tissues has not been completely studied. Undesirable effects of bismuth include anemia which could result from suicidal erythrocyte death or eryptosis. The objective of this research was to determine the effect of bismuth dimercaptopropanol nanoparticles on blood cells. The nanoparticles are composed of 53 nm crystallites on average and have a spherical structure, agglomerating into clusters of small nanoparticles. Based on cell viability assays and optical microscopy, cytotoxicity on erythrocytes was observed after growing with 500 and 1000 µM of BisBAL NPs for 24 h. AM Calcein was retained inside erythrocytes when they were exposed to 100 µM (or lower concentrations) of BisBAL NPs for 24 h, suggesting the absence of damage in plasmatic membrane. Genotoxic assays revealed no damage to genomic DNA of blood cells after 24 h of exposition to BisBAL NPs. Finally, 100–1000 µM of bismuth nanoparticles promotes apoptosis between blood cells after 24 h of incubation. Hence BisBAL NPs at concentrations lower than 100 µM do not cause damage on blood cells; they could potentially be used by humans without affecting erythrocytes and leukocytes.

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Triggering of Programmed Erythrocyte Death by Alantolactone

Cited by 7 publications

References 97 publications

Indolic Uremic Solutes Enhance Procoagulant Activity of Red Blood Cells through Phosphatidylserine Exposure and Microparticle Release

Indolic Uremic Solutes Enhance Procoagulant Activity of Red Blood Cells through Phosphatidylserine Exposure and Microparticle Release

Induction of Eryptosis in Red Blood Cells Using a Calcium Ionophore

Effect of Lipophilic Bismuth Nanoparticles on Erythrocytes

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