MicroRNA-294 Regulates Apoptosis of the Porcine Cerebellum Caused by Selenium Deficiency via Targeting iNOS

Deficiency of the essential trace element selenium (Se) can lead to cell apoptosis, and various microRNAs (miRNAs) are known to participate in the regulation of apoptosis by regulating their target genes. In this study, we explore the effect of Se deficiency on porcine cerebellar cell apoptosis and the role of miRNA in this process. After constructing a low-Se pig model, we observed the porcine cerebellum through an electron microscope and observed obvious characteristics of apoptosis. Moreover, it was found that the expression of miR-294 in Se-deficient pigs was significantly lower than that in the control group. Through bioinformatics, qRT-PCR, western blot analysis, and other experimental techniques, we further confirmed that inducible nitric oxide synthase (iNOS) is one of the target genes of miR-294. Our experimental results show that Se deficiency can reduce the expression of miR-294 and increase both the expression of iNOS and the nitric oxide (NO) content (P < 0.01). The expression of heat shock proteins (HSPs, such as HSP70, HSP90, HSP60, HSP40, and HSP27) and mitochondrial pathway-related indicators, such as Bcl2-associated X protein (Bax), cytochrome C (Cyt-C), and cysteinyl aspartate-specific proteinases (caspase 3, caspase 7, and caspase 8), was upregulated (P < 0.05), and the expression of B cell lymphoma-2 (Bcl-2) was downregulated (P < 0.05). In summary, we believe that Se deficiency can lead to abnormal expression of miR-294 and HSPs; moreover, the mitochondrial apoptosis pathway is activated, which significantly enhances apoptosis of cerebellar cells in Se-deficient pigs. These results enrich the biological effects of Se deficiency.

Automated summary

The deficiency of the essential trace element selenium can lead to cell apoptosis, and miR-294 and HSPs play important roles in this process. Activation of the mitochondrial apoptosis pathway significantly enhances apoptosis of cerebellar cells in Se-deficient pigs. These findings enrich our understanding of the biological effects of Se deficiency.