Open AccessWIN 55,212-2 shows anti-inflammatory and survival properties in human iPSC-derived cardiomyocytes infected with SARS-CoV-2
Author(s) -
Luiz Guilherme H.S. Aragão,
Jonice Oliveira,
Jairo R. Temerozo,
Mayara Abud Mendes,
José Alexandre Salerno,
Carolina Pedrosa,
Teresa PuigPijuan,
Carla Pires Veríssimo,
Isis Moraes Ornelas,
Thayana Torquato,
Gabriela Vitória,
Carolina Q. Sacramento,
Natália Fintelman-Rodrigues,
Suelen da Silva Gomes Dias,
Vinícius Cardoso Soares,
Letícia R. Q. Souza,
Karina Karmirian,
Livia GotoSilva,
Diogo Biagi,
Estela Cruvinel,
Rafael Dariolli,
Daniel Rodrigues Furtado,
Patrı́cia T. Bozza,
Helena L. Borges,
Thiago Moreno L. Souza,
Marília Zaluar P. Guimarães,
Stevens K. Rehen
Publication year - 2021
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.12262
Subject(s) - cytokine storm , inflammation , coronavirus , tumor necrosis factor alpha , cytokine , lactate dehydrogenase , medicine , agonist , immunology , pharmacology , receptor , biology , disease , covid-19 , enzyme , infectious disease (medical specialty) , biochemistry
Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), which can infect several organs, especially impacting respiratory capacity. Among the extrapulmonary manifestations of COVID-19 is myocardial injury, which is associated with a high risk of mortality. Myocardial injury, caused directly or indirectly by SARS-CoV-2 infection, can be triggered by inflammatory processes that lead to damage to the heart tissue. Since one of the hallmarks of severe COVID-19 is the “cytokine storm”, strategies to control inflammation caused by SARS-CoV-2 infection have been considered. 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) in human iPSC-derived cardiomyocytes (hiPSC-CMs) infected with SARS-CoV-2. WIN did not modify angiotensin-converting enzyme II protein levels, nor reduced viral infection and replication in hiPSC-CMs. On the other hand, WIN reduced the levels of interleukins six, eight, 18 and tumor necrosis factor-alpha (TNF-α) released by infected cells, and attenuated cytotoxic damage measured by the release of lactate dehydrogenase (LDH). Our findings suggest that cannabinoids should be further explored as a complementary therapeutic tool for reducing inflammation in COVID-19 patients.