miR-210/NF-κB axis: A new direction for regulating cadmium-induced pig artery inflammatory injury

Cadmium (Cd) is a toxic metal pollutant that still exists in the environment. The microRNA (miRNA) is a type of noncoding RNA that plays an important role in gene posttranscriptional regulation and disease development. Although the toxic effects of Cd have been extensively studied, studies on the mechanism of Cd from the perspective of miRNA are still limited. So, we established a Cd-exposure pig model, which confirmed that Cd exposure would cause pig artery damage. The miR-210 with the most reduced expression and the nuclear factor kappa B (NF-?B) that had a targeting relationship with miR-210 were screened. The effect of miR-210/NF-?B on the artery damage induced by Cd exposure was investigated by acridine orange/ethidium bromide staining, reactive oxygen species (ROS) staining, quantitative PCR, and western blotting. The results showed that miR-210 inhibitor, pcDNA-NF-?B could induce ROS overproduction in pig hip artery endothelial cells, thus inducing Th1/Th2 imbalance and necroptosis, leading to increased inflammation, while small interfering RNA-NF-?B played a mitigating role. In conclusion, Cd can induce artery necroptosis and Th1/Th2 imbalance by regulating the miR-210/NF-?B axis, so as to lead to artery inflammatory damage. In this study, we explored the way in which Cd exposure causes artery damage in pig, providing a new perspective on the regulatory damage of miR-210/NF-?B axis.

Automated summary

This study established a Cd-exposure pig model and found that Cd exposure can cause artery damage. The downregulated expression of miR-210 and its targeting relationship with NF-κB were screened. The effect of miR-210/NF-κB on Cd-induced artery damage was investigated, revealing that Cd can induce artery necroptosis and Th1/Th2 imbalance through the regulation of the miR-210/NF-κB axis, leading to artery inflammatory damage.