Overexpression of miR-192 Inhibits In Vitro Porcine Embryo Development by Inducing Oxidative Stress Damage and Impairing Mitochondrial Function.

Early embryonic development relies on intricately regulated gene expression, and miRNAs influence zygotic genome activation (ZGA), cleavage, and cell fate determination through post-transcriptional regulatory mechanisms. miR-192 is expressed in early pig embryos and participates in various reproductive processes. However, its role in pre-implantation pig embryo development remains poorly understood. In this study, we microinjected the miR-192 agonist (miR-192 agomir) into parthenogenetically activated pig embryos to evaluate its effects on early pig embryo development. Our findings indicate that compared to the control group (agomir NC), miR-192 agomir impairs the developmental capacity of parthenogenetic pig embryos to reach the 2-cell, 4-cell, and blastocyst stages. This impairment leads to imbalances in the oxidative-reductive system and abnormalities in mitochondrial function during the 4-cell stage, resulting in the significant accumulation of ROS, notable decreases in the expression of antioxidant enzymes CAT and SOD1 mRNA, reduction in mitochondrial membrane potential, and induction of apoptosis in pig blastocysts. Additionally, the overexpression of miR-192 inhibits the expression of its target genes YY1 and the pluripotency factor NANOG mRNA. In conclusion, this study reveals that the overexpression of miR-192 adversely affects early pig embryo development, providing new evidence for understanding the role miR-192 plays in reproduction.