Endothelial injury, hyperactivation and intensification of pro-inflammatory and coagulant factors are well known severe symptoms of SARS-CoV-2 infection. These clinical conditions may contribute to increased circulating microparticles, membranous structures released from apoptotic or activated cells, which can carry bioactive molecules that could induce vascular responses such as endothelial dysfunction and oxidative stress. Studies demonstrate that between 40 and 80% of recovered patients from SARS-CoV-2 infection develop cardiovascular complications that could persist for 12 months after the diagnosis. Besides, endothelial dysfunction is a potential mechanism involved in persisting cardiovascular sequels after COVID-19. In that way, we developed the hypothesis that MP produced during the coronavirus infection could contribute to endothelial dysfunction on long COVID-19. Thus, circulating MP were isolated from patients that had severe COVID-19 and were hospitalized on Hospital de Clínicas da Unicamp (clinical assay ITHACA - PMID 33472675), 1, 4 and 24 weeks after hospital discharge. The isolated MP will be added to endothelial cells in vitro to evaluate genetic and protein expression of pro-inflammatory factors, leukocyte adhesion molecules, components of renin-angiotensin system, reactive oxygen species, nitric oxide and prostanoids production.
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