TY - JOUR
T1 - WIN 55,212-2 shows anti-inflammatory and survival properties in human iPSC-derived cardiomyocytes infected with SARS-CoV-2
AU - Aragão, Luiz Guilherme H.S.
AU - Oliveira, Júlia T.
AU - Temerozo, Jairo R.
AU - Mendes, Mayara A.
AU - Salerno, José Alexandre
AU - Pedrosa, Carolina S.G.
AU - Puig-Pijuan, Teresa
AU - Veríssimo, Carla P.
AU - Ornelas, Isis M.
AU - Torquato, Thayana
AU - Vitória, Gabriela
AU - Sacramento, Carolina Q.
AU - Fintelman-Rodrigues, Natalia
AU - Da Silva Gomes Dias, Suelen
AU - Soares, Vinicius Cardoso
AU - Souza, Letícia R.Q.
AU - Karmirian, Karina
AU - Goto-Silva, Livia
AU - Biagi, Diogo
AU - Cruvinel, Estela M.
AU - Dariolli, Rafael
AU - Furtado, Daniel R.
AU - Bozza, Patrícia T.
AU - Borges, Helena L.
AU - Souza, Thiago M.L.
AU - Guimarães, Marília Zaluar P.
AU - Rehen, Stevens K.
N1 - Publisher Copyright:
© 2021 PeerJ Inc.. All rights reserved.
PY - 2021/10
Y1 - 2021/10
N2 - 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-a) 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.
AB - 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-a) 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.
KW - COVID-19
KW - Cannabinoids
KW - Human iPSC-derived cardiomyocytes
KW - SARS-Cov-2
KW - WIN 55,212-2
UR - https://www.scopus.com/pages/publications/85116878703
U2 - 10.7717/peerj.12262
DO - 10.7717/peerj.12262
M3 - Article
AN - SCOPUS:85116878703
SN - 2167-8359
VL - 9
JO - PeerJ
JF - PeerJ
M1 - e12262
ER -