CD235a (Glycophorin‐A) Is the Most Predictive Value Among Different Circulating Cellular Microparticles in Thrombocytopenic Human Immunodeficiency Virus Type 1

El-Menshawy, Nadia; Eissa, Mohamed M.; Farag, Raghada; Aboalyazed, Ahmed

doi:10.1002/jcla.21842

Cited by 7 publications

(7 citation statements)

References 49 publications

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“…ErMPs have also emerged as potential mediators of transfusion‐related morbidity by thrombin‐dependent activation of the complement system . Moreover, CD235a + ErMPs are sensitive predictors of thrombotic events in thrombocytopenic HIV patients . However, the physiologic role of ErMPs has not been fully elucidated.…”

Section: Discussionmentioning

confidence: 99%

Growing thrombi release increased levels of CD235a+ microparticles and decreased levels of activated platelet‐derived microparticles. Validation in ST‐elevation myocardial infarction patients

Suades¹,

Padró²,

Vilahur³

et al. 2015

Journal of Thrombosis and Haemostasis

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increased levels of CD235a + microparticles and decreased levels of activated platelet-derived microparticles. Validation in ST-elevation myocardial infarction patients. J Thromb Haemost 2015; 13: 1776-86.Summary. Background: Local fluid dynamics and exposed atherosclerotic lesions regulate thrombus formation. Activated cells in the attached thrombi release microparticles to the circulation (circulating microparticles [cMPs]); however, their phenotype is unknown. Objectives: To investigate the specific phenotype of the cMPs released by growing thrombi. Methods/patients: cMPs released by thrombi growing in different well-characterized thrombogenic conditions were investigated. cMP contents just before and immediately after perfusion of the thrombogenic surfaces were analyzed by triple-labeling flow cytometry. cMPs were tested for their thrombin-generating capacity. The cMPs identified in the ex vivo perfusion experiments were validated in blood of ST-elevation myocardial infarction (STEMI) patients undergoing thrombectomy and percutaneous coronary intervention. Culprit coronary blood (STEMI-CCB) and peripheral artery blood (STEMI-PAB) were simultaneously analyzed and compared with peripheral artery blood from agematched controls (C-PAB) and peripheral artery blood from patients who had recovered from acute coronary syndrome (ACS) (pSTEMI-PAB). Results: The levels of annexin V + cMPs significantly increased in blood collected after perfusion of the exposed thrombogenic surfaces. cMP release was directly related to the formed thrombus mass and the plasma procoagulant activity. Post-thrombus blood showed higher thrombin generation potential and contained higher levels of cMPs carrying glycophorin-A (CD235a + ; erythrocyte-derived microparticles [ErMPs]) than preperfusion blood (P < 0.05), whereas the levels of cMPs carrying activated and adhesion platelet markers were decreased. STEMI-CCB and STEMI-PAB had significantly higher ErMP levels than control blood (P < 0.005). ErMP levels were also significantly higher in STEMI-PAB than in pSTEMI-PAB, validating the experimental mechanistic studies and suggesting that ErMPs are markers of ongoing coronary thrombosis (C-statistics: 0.950; 95% confidence interval 0.889-1.000; P < 0.001). Conclusion: Glycophorin-A-rich microparticles are released from evolving growing thrombi into the distal perfusing blood, and can be measured in peripheral blood. CD235a + cMPs may constitute a novel systemic biomarker of ongoing thrombosis.

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Section: Discussionmentioning

confidence: 99%

Growing thrombi release increased levels of CD235a+ microparticles and decreased levels of activated platelet‐derived microparticles. Validation in ST‐elevation myocardial infarction patients

Suades¹,

Padró²,

Vilahur³

et al. 2015

Journal of Thrombosis and Haemostasis

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“…(17) Thus, an intense and persistent activation of platelets/microparticles can contribute to increased vascular risks which underlie HIV-associated endothelial dysfunction with thrombotic events and vascular diseases. (18,19,20) Therefore, our findings emphasise that an increased oxidative stress in platelets and P-MPs may increase the risk of RF during HIV-TB coinfection.…”

Section: Proof Proof Proofmentioning

confidence: 64%

Increased levels of reactive oxygen species in platelets and platelet-derived microparticles and the risk of respiratory failure in HIV/AIDS patients

Gama

Oliveira

Chaves

et al. 2020

Mem. Inst. Oswaldo Cruz

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Respiratory failure (RF) is the main cause of hospital admission in HIV/AIDS patients. This study assessed comorbidities and laboratory parameters in HIV/AIDS inpatients with RF (N = 58) in relation to those without RF (N = 36). Tuberculosis showed a huge relative risk and platelet counts were slightly higher in HIV/AIDS inpatients with RF. A flow cytometry assay for reactive oxygen species (ROS) showed lower levels in platelets of these patients in relation to the healthy subjects. However, when stimulated with adrenaline, ROS levels increased in platelets and platelet-derived microparticles of HIV/AIDS inpatients, which may increase the risk of RF during HIV and tuberculosis (HIV-TB) coinfection.

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“…The TF on PEVs could originate from the platelet or its uptake from TF-bearing EVs of other cellular origins [ 132 ]. Alternatively, PEVs can affect coagulation through the activation of other cells to induce a pro-thrombotic environment [ 53 , 57 , 58 , 103 , 105 , 120 , 121 , 133 , 134 , 135 , 136 , 137 , 138 , 139 , 140 , 141 , 142 , 143 , 144 , 145 ] ( Figure 5 ). As an example, Terrisse et al found that PEVs will adhere to endothelial cells dependent on lactadherin, PS, and αVβ3 integrin.…”

Section: Platelet-derived Extracellular Vesicles Under Disease Condit...mentioning

confidence: 99%

“…HIV Tat1 directly activates platelets through chemokine receptor 3 (CCR3) and β3-integrin, resulting in PEV formation [ 191 ]. Correspondingly, patients with HIV have increased numbers of PEVs in their blood [ 9 , 58 , 76 , 192 ], though the numbers of PEVs detected are again variable in different reports. Hijmans et al found 40 PEVs per µL plasma in healthy individuals and 140 PEVs per µL plasma in HIV patients [ 76 ], while Falasca et al found 897 annexin V negative and 112 annexin V positive PEVs per µL plasma in healthy individuals and 1419 annexin V negative and 215 annexin V positive PEVs per µL plasma in HIV patients [ 192 ].…”

Section: Platelet-derived Extracellular Vesicles In Infectious Diseasesmentioning

confidence: 99%

The Role of Platelet-Derived Extracellular Vesicles in Immune-Mediated Thrombosis

Eustes

Dayal

2022

IJMS

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Platelet-derived extracellular vesicles (PEVs) play important roles in hemostasis and thrombosis. There are three major types of PEVs described based on their size and characteristics, but newer types may continue to emerge owing to the ongoing improvement in the methodologies and terms used to define various types of EVs. As the literature on EVs is growing, there are continuing attempts to standardize protocols for EV isolation and reach consensus in the field. This review provides information on mechanisms of PEV production, characteristics, cellular interaction, and their pathological role, especially in autoimmune and infectious diseases. We also highlight the mechanisms through which PEVs can activate parent cells in a feedback loop.

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CD235a (Glycophorin‐A) Is the Most Predictive Value Among Different Circulating Cellular Microparticles in Thrombocytopenic Human Immunodeficiency Virus Type 1

Abstract: Different cellular MPs and platelets activated in HIV patients could have a role in thrombotic events in these patients.

Cited by 7 publications

References 49 publications

Growing thrombi release increased levels of CD235a+ microparticles and decreased levels of activated platelet‐derived microparticles. Validation in ST‐elevation myocardial infarction patients

Growing thrombi release increased levels of CD235a+ microparticles and decreased levels of activated platelet‐derived microparticles. Validation in ST‐elevation myocardial infarction patients

Increased levels of reactive oxygen species in platelets and platelet-derived microparticles and the risk of respiratory failure in HIV/AIDS patients

The Role of Platelet-Derived Extracellular Vesicles in Immune-Mediated Thrombosis

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