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MicroRNA‐223 triggers inflammation in porcine aorta by activating NLRP3 inflammasome under selenium deficiency
Author(s) -
Qing Zhang,
Kaixin Zhang,
Yanfei Han,
Yiming Zhang,
Hua Xue,
Ling Zhou,
Guangliang Shi,
Shu Li
Publication year - 2021
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.30178
Subject(s) - gene knockdown , inflammation , inflammasome , selenium deficiency , microrna , apoptosis , messenger rna , downregulation and upregulation , receptor , biology , microbiology and biotechnology , chemistry , cancer research , immunology , endocrinology , oxidative stress , gene , biochemistry , superoxide dismutase , glutathione peroxidase
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.