Platelet-Released Extracellular Vesicle Characteristics Differ in Chronic and in Acute Heart Disease

Author:

Vilella-Figuerola Alba12ORCID,Cordero Alberto345ORCID,Mirabet Sònia56ORCID,Muñoz-García Natàlia1ORCID,Suades Rosa1ORCID,Padró Teresa15ORCID,Badimon Lina157ORCID

Affiliation:

1. Cardiovascular Program-ICCC, Institut d'Investigació Biomèdica Sant Pau (IIB SANT PAU), Barcelona, Spain

2. Biochemistry and Molecular Biology Department, Universitat Autònoma de Barcelona (UAB), Cerdanyola del Vallès, Spain

3. Cardiology Department, Hospital Universitario de San Juan, Alicante, Spain

4. Unidad de Investigación en Cardiología, Fundación para el Fomento de la Investigación Sanitaria y Biomédica de la Comunitat Valenciana (FISABIO), València, Spain

5. Centro de Investigación Biomédica en Red Cardiovascular (CIBER-CV), Instituto de Salud Carlos III, Madrid, Spain

6. Heart Failure Group, Cardiology Department, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain

7. UAB-Chair Cardiovascular Research, Barcelona, Spain

Abstract

Background Extracellular vesicles (EVs), shed in response to cell activation, stress, or injury, are increased in the blood of patients with cardiovascular disease. EVs are characterized by expressing parental-cell antigens, allowing the determination of their cellular origin. Platelet-derived EVs (pEVs) are the most abundant in blood. Although not universally given, EVs generally express phosphatidylserine (PS) in their membrane. Objectives To investigate pEVs in chronic and acute conditions, such as chronic heart failure (CHF) and first-onset acute coronary syndrome (ACS), in patients treated as per guidelines. Methods EVs in CHF patients (n = 119), ACS patients (n = 58), their respective controls (non-CHF [n = 21] and non-ACS [n = 24], respectively), and a reference control group (n = 31) were characterized and quantified by flow cytometry, using monoclonal antibodies against platelet antigens, and annexin V (AV) to determine PS exposure. Results CHF patients had higher EVs-PS− numbers, while ACS had predominantly EVs-PS+. In contrast to ACS, CHF patients had significantly reduced numbers of pEVs carrying PECAM and αIIb-integrin epitopes (CD31+/AV+, CD41a+/AV+, and CD31+/CD41a+/AV+), while no differences were observed in P-selectin-rich pEVs (CD62P+/AV+) compared with controls. Additionally, background etiology of CHF (ischemic vs. nonischemic) or ACS type (ST-elevation myocardial infarction [STEMI] vs. non-STEMI [NSTEMI]) did not affect pEV levels. Conclusion PS exposure in EV and pEV-release differ between CHF and ACS patients, with tentatively different functional capacities beyond coagulation to inflammation and cross-talk with other cell types.

Publisher

Georg Thieme Verlag KG

Subject

Hematology

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