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MicroRNA‐223 triggers inflammation in porcine aorta by activating NLRP3 inflammasome under selenium deficiency

Qing Zhang, Zhang Kaixin, Han Yanfei, Yiming Zhang, Xue Hua, Ling Zhou, Shi Guangliang, Shu Li

2020Journal of Cellular Physiology21 citationsDOI

Abstract

Selenium (Se) is an essential trace element in organism. Se deficiency can cause many diseases, including vascular disease. Studies have shown that inflammation is the main inducement of vascular disease, microRNA (miRNA) can influence inflammation in various ways, and Se deficiency can affect miRNAs expression. To study the mechanism of aorta damage caused by Se deficiency, we constructed a Se deficiency porcine aorta model and found that Se deficiency can significantly inhibit miR-223, which downregulates the expression of nucleotide-binding oligomerization domain-like receptor family 3 (NLRP3). Subsequently, we found that in Se deficiency group, NLRP3, and its downstream (caspase-1, apoptosis-related spot-like protein [ASC], IL-18, IL-1β) expression was significantly increased. In vitro, we cultured pig iliac endothelium cell lines, and constructed miR-223 knockdown and overexpression models. NLRP3 messenger RNA and protein levels were significant increased in the knockdown group, and decreased in the overexpression group. The results of this study show that Se deficiency in porcine arteries can induce inflammation through miR-223/NLRP3.

Topics & Concepts

Gene knockdownInflammationInflammasomeSelenium deficiencymicroRNAApoptosisDownregulation and upregulationMessenger RNAReceptorBiologyCell biologyChemistryCancer researchImmunologyInternal medicineEndocrinologyOxidative stressMedicineGeneBiochemistrySuperoxide dismutaseGlutathione peroxidaseSelenium in Biological SystemsBiomarkers in Disease MechanismsInflammasome and immune disorders