Anti-IL-1β platelet microparticles protected cardiomyocytes from apoptosis by neutralizing IL-1β and decreasing caspase-3 activity after acute myocardial infarction.
Do anti-IL-1β platelet microparticles protect cardiomyocytes from apoptosis and prevent adverse cardiac remodeling in acute myocardial infarction?
Targeted delivery of anti-IL-1β antibodies via platelet microparticles is a promising strategy to reduce inflammation and promote cardiac repair after myocardial infarction.
An acute myocardial infarction (AMI) induces a sterile inflammatory response that facilitates further heart injury and promotes adverse cardiac remodeling. Interleukin-1β (IL-1β) plays a central role in the sterile inflammatory response that results from AMI. Thus, IL-1β blockage is a promising strategy for treatment of AMI. However, conventional IL-1β blockers lack targeting specificity. This increases the risk of serious side effects. To address this problem herein, we fabricated platelet microparticles (PMs) armed with anti-IL-1β antibodies to neutralize IL-1β after AMI and to prevent adverse cardiac remodeling. Our results indicate that the infarct-targeting PMs could bind to the injured heart, increasing the number of anti-IL-1β antibodies therein. The anti-IL-1β platelet PMs (IL1-PMs) protect the cardiomyocytes from apoptosis by neutralizing IL-1β and decreasing IL-1β-driven caspase-3 activity. Our findings indicate that IL1-PM is a promising cardiac detoxification agent that removes cytotoxic IL-1β during AMI and induces therapeutic cardiac repair.
Li et al. (Thu,) conducted a other in Acute myocardial infarction. Anti-IL-1β platelet microparticles (IL1-PMs) was evaluated on Cardiomyocyte apoptosis and IL-1β-driven caspase-3 activity. Anti-IL-1β platelet microparticles protected cardiomyocytes from apoptosis by neutralizing IL-1β and decreasing caspase-3 activity after acute myocardial infarction.
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