RETRACTED ARTICLE: Downregulation of miR-483-5p decreases hypoxia-induced injury in human cardiomyocytes by targeting MAPK3

Abstract

Background: MiR-483-5p was recently identified as a risk factor in the early stages of acute myocardial infarction (AMI) patients. Here, we further investigated how miR-483-5p affects cardiomyocyte apoptosis and oxidative stress under hypoxic conditions. Methods: Plasma samples were collected from AMI patients and healthy volunteers. The expression of miR-483-5p was determined using quantitative real-time PCR. An in vitro hypoxic model was constructed to mimic AMI in AC16 cells. Cell viability, apoptosis and oxidative stress biomarker levels (MDA, SOD and CAT) were respectively determined using CCK-8, flow cytometry and commercial assay kits. Results: The expression levels of miR-483-5p were significantly higher in AMI patients than in control subjects. Circulating levels of miR-483-5p positively correlated with creatine kinase MB isoform (CK-MB) and cardiac troponin I (cTnI) levels. The in vitro experiments showed that the expression levels of miR-483-5p were also upregulated in hypoxia-induced AC16 cell injury. MiR-483-5p overexpression significantly increased hypoxia-induced cardiomyocyte apoptosis and oxidative stress, while knockdown attenuated these effects. Mechanistically, miR-483-5p directly targets MAPK3 in AC16 cells. Furthermore, the protective effects of miR-483-5p knockdown against hypoxiainduced cardiomyocyte injury are partially dependent on MAPK3. Conclusions: MiR-483-5p, which targets MAPK3, might be a potential therapeutic target for the diagnosis and prevention of hypoxia-induced myocardial injury.

Amniotic Fluid microRNA in Severe Twin-Twin Transfusion Syndrome Cardiomyopathy—Identification of Differences and Predicting Demise

“…Within the realm of cardiovascular disease, we found differential expression of miR-484, miR-433, miR-320 and miR-383-5p, all of which have previously been documented to play an important role in the heart's response to ischemia/reperfusion injury [40][41][42][43]. Additionally, miR-484-5p and miR-484-3p are suggested as potential therapeutic targets to limit hypoxia-induced myocardial injury [44,45]. Other differentially expressed miRNAs are also associated with cardiac disease; miR-134 is elevated in early stages of myocardial infarction and its inhibition can decrease apoptosis of cardiomyocytes [46,47].…”

Genome-Wide Analysis of LncRNA in Bovine Mammary Epithelial Cell Injuries Induced by Escherichia Coli and Staphylococcus Aureus

“…The MAPK signaling pathway is closely related to cell injury [ 53 ]. For example, MAPK3, also known as extracellular-regulated protein kinase 1 (ERK1), is reported to downregulate the expression of miR-483-5p post-transcriptionally, leading to apoptosis and oxidative stress in human cardiomyocytes under hypoxia [ 54 ]. Another study reported that inhibiting miR-124 can cause the overexpression of MAPK14, which, in turn, activates the MAPK signaling pathway and promotes lung cell apoptosis and inflammation [ 55 ].…”

Integrative Analysis of Key Genes and Signaling Pathways By Bioinformatics in Patients with Type 1 Diabetes Mellitus Combined with Acute Myocardial Infarction

“…The occurrence of myocardial infarction in patients with type I diabetes may be related to mitochondrial dysfunction, so erbB2 is also a highly correlated gene [32] . The MAPK3 pathway is involved in the repair of myocardial ischemia [33,34,35] . This may be related to the body's self-repair after acute myocardial infarction, which may provide a target for future treatment.…”