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Abstract
BackgroundAberrant circular RNAs (circRNAs) expression is closely associated with cardiovascular diseases. However, the regulatory functions of circRNAs in myocardial ischemia-reperfusion (I/R) injury remain largely undefined. MethodsWe established myocardial I/R model in vitro by oxygen and glucose deprivation and reperfusion in cardiomyocytes. The expression of circ_0050908, microRNA (miR)-324-5p, and TNF receptor-associated factor (TRAF3) was detected using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blot. The apoptosis was assayed by flow cytometry and Western blot. The activity of interleukin (IL)-1β, IL-6, tumor necrosis factor (TNF-α), lactate dehydrogenase (LDH), creatine kinase myocardial band (CK-MB), CK, and superoxide dismutase (SOD) was evaluated using the relative commercial kits. Reactive oxygen species (ROS) detection was conducted using Dihydroethidium (DHE) staining. The interactions between miR-324-5p and circ_0050908 or TRAF3 were determined by dual-luciferase activity, RNA immunoprecipitation (RIP), and pull-down assays. ResultsI/R stimulation up-regulated circ_0050908 expression in cardiomyocytes. Functional experiments suggested that circ_0050908 knockdown led to the rescue of apoptosis enhancement, inflammation, and oxidative stress induced by I/R in cardiomyocytes. Mechanistically, circ_0050908 directly targeted miR-324-5p, and miR-324-5p inhibition reversed the inhibitory action of circ_0050908 knockdown on myocardial I/R injury. TRAF3 was verified to be a target of miR-324-5p, and miR-324-5p suppressed I/R-induced apoptosis, inflammatory response, and oxidative stress in cardiomyocytes through TRAF3. Besides that, circ_0050908 could regulate TRAF3 expression by miR-324-5p. ConclusionCirc_0050908 knockdown protects cardiomyocytes against I/R injury by reducing apoptosis, inflammatory response, and oxidative stress through miR-324-5p/TRAF3 axis, revealing a novel therapeutic strategy for preventing myocardial I/R injury.
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