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

J Cell Physiol. 2021 Jun;236(6):4555-4564. doi: 10.1002/jcp.30178. Epub 2020 Nov 25.

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.

Keywords: NLRP3; microRNA-223; porcine; selenium deficient; vascular injury.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

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

Substances

  • CARD Signaling Adaptor Proteins
  • Inflammasomes
  • Interleukin-18
  • Interleukin-1beta
  • MicroRNAs
  • NLR Family, Pyrin Domain-Containing 3 Protein
  • Caspase 1
  • Selenium