关键词: NLRP3 microRNA-223 porcine selenium deficient vascular injury

Mesh : Animal Feed Animal Nutritional Physiological Phenomena Animals Aorta / immunology metabolism pathology Aortitis / genetics immunology metabolism pathology CARD Signaling Adaptor Proteins / genetics metabolism Caspase 1 / genetics metabolism Cells, Cultured Disease Models, Animal Endothelial Cells / immunology metabolism pathology Inflammasomes / genetics metabolism Interleukin-18 / genetics metabolism Interleukin-1beta / genetics metabolism MicroRNAs / genetics metabolism NLR Family, Pyrin Domain-Containing 3 Protein / genetics metabolism Selenium / deficiency Signal Transduction Sus scrofa

来  源:   DOI:10.1002/jcp.30178   PDF(Sci-hub)

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.
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