WIN 55,212-2 shows anti-inflammatory and survival properties in human iPSC-derived cardiomyocytes infected with SARS-CoV-2
2021
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.
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