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SARS-CoV-2 proteins

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    A cannabinoid receptor agonist shows anti-inflammatory and survival properties in human SARS-CoV-2-infected iPSC-derived cardiomyocytes MESHD

    Authors: Luiz Guilherme H.S. Aragao; Julia T Oliveira; Jairo R Temerozo; Mayara A Mendes; Jose Alexandre Salerno; Carolina da S. G. Pedrosa; Teresa Puig-Pijuan; Carla Verissimo; Isis M Ornelas; Thayana Torquato; Gabriela Vitoria; Carolina Q. Sacramento; Natalia Fintelman-Rodrigues; Suelen da Silva Gomes Dias; Vinicius Cardoso Soares; Leticia R. Q. Souza; Karina Karmirian; Livia Goto-Silva; Diogo Biagi; Estela M. Cruvinel; Rafael Dariolli; Daniel R. Furtado; Patricia T. Bozza; Helena L. Borges; Thiago Moreno L. Souza; Marilia Zaluar P. Guimaraes; Stevens Rehen

    doi:10.1101/2021.02.20.431855 Date: 2021-02-21 Source: bioRxiv

    Coronavirus disease 2019 MESHD ( COVID-19 MESHD) is caused by acute respiratory syndrome coronavirus 2 MESHD (SARS-CoV-2), which can infect several organs and lead to loss of vital organ function, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 MESHD is myocardial injury MESHD, caused both directly and indirectly by SARS-CoV-2, and which is associated with a high risk of mortality. One of the hallmarks of severe COVID-19 MESHD is the "cytokine storm", at which point the immune system malfunctions, leading to possible organ failure MESHD and death MESHD. Cannabinoids are known to have anti-inflammatory properties by negatively modulating the release of pro-inflammatory cytokines. Herein, we investigated the effects of the cannabinoid agonist WIN 55,212-2 (WIN) on SARS-CoV-2-infected MESHD human iPSC-derived cardiomyocytes (hiPSC-CMs). Although WIN did not modulate angiotensin-converting enzyme II, nor reduced SARS-CoV-2 infection MESHD and replication in hiPSC-CMs at the conditions tested, it had anti-inflammatory and protective effects by reducing the levels of interleukins 6, 8,18 and tumor necrosis factor-alpha HGNC tumor necrosis factor-alpha MESHD ( TNF HGNC-) and lactate dehydrogenase (LDH) activity in these cells without causing hypertrophic cardiac damage MESHD. These findings suggest that cannabinoids should be further investigated as an alternative therapeutic tool for the treatment of COVID-19 MESHD. HighlightsO_LIHuman iPSC-derived cardiomyocytes (hiPSC-CMs) express CB1 HGNC receptor. C_LIO_LIThe cannabinoid receptor agonist, WIN 55,212-2 (WIN), does not influence SARS-CoV-2 infection MESHD in hiPSC-CMs. C_LIO_LIWIN reduces inflammation MESHD and death MESHD in SARS-CoV-2-infected hiPSC-CMs MESHD. C_LI

    The Pathogenisis of COVID-19 MESHD Myocardial Injury: an Immunohistochemical Study of Postmortem Biopsies 

    Authors: Camila Hartmann; Anna Flavia dos Santos Miggiolaro; Jarbas da Silva Motta Junior; Lucas Baena Carstens; Caroline Busatta Vaz De Paula; Sarah Fagundes Grobe; Larissa Hermann de Souza Nunes; Gustavo Lenci Marques; Lidia Zytynski Moura; Lucia de Noronha; Cristina Pellegrino Baena

    doi:10.21203/rs.3.rs-45192/v2 Date: 2020-07-17 Source: ResearchSquare

    Rationale: M yocardial injury MESHDis significantly and independently associated with mortality in COVID-19 MESHD patients. However, the pathogenesis of m yocardial injury MESHDin COVID-19 MESHD is still not clear, and cardiac involvement by SARS-CoV-2 remains a major challenge worldwide. Objective: This histopathological and immunohistochemical study seeks to clarify the pathogenesis and propose a mechanism with pathways involved in COVID-19 MESHD m yocardial injury. MESHD Methods and Results: Postmortem minimally invasive autopsies were performed in six patients who died from COVID-19 MESHD, and the myocardium samples were compared to a control patient. Histopathological analysis was performed using hematoxylin-eosin and toluidine blue staining. Immunohistochemical (IHC) staining was performed using monoclonal antibodies against the following targets: c aspase-1, HGNC I CAM-1, HGNC T NF-α, HGNC I L-4, HGNC I L-6, HGNC C D163, HGNC T GF-β, HGNC M MP-9, HGNC type 1 and type 3 collagen. The samples were also subjected to a TUNEL assay to detect potential apoptosis. The histopathological analysis showed severe pericellular interstitial e dema MESHDsurrounding each of the cardiomyocytes and higher mast cells count by high-power field in all COVID-19 MESHD myocardium samples. The IHC analysis showed increased expression of c aspase-1, HGNC I CAM-1, HGNC I L-4, HGNC I L-6, HGNC C D163, HGNC M MP-9 HGNCand type 3 collagen in the COVID-19 MESHD patients compared to the control. No difference from the control was observed in expression of T NF-α, HGNC T GF-β HGNCand type 1 collagen. The TUNEL assay was positive in all the COVID-19 MESHD samples confirming the presence of endothelial apoptosis. Conclusions: The pathogenesis of COVID-19 MESHD m yocardial injury MESHDseems to be related with pyroptosis leading to endothelial cell injury and disfunction. The subsequent i nflammation MESHDwith associated interstitial e dema MESHDcould explain the myocardial disfunction and a rrythmias MESHDin these patients. Our findings also show that COVID-19 MESHD m yocardial injury MESHDmay cause m yocardial fibrosis MESHDin the long term. These patients should be monitored for m yocardial dysfunction MESHDand a rrythmias MESHDafter the acute phase of COVID-19 MESHD.

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MeSH Disease
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SARS-CoV-2 Proteins


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