LncRNA MIAT regulated by selenium and T-2 toxin increases NF-κB-p65 activation, promoting the progress of Kashin-Beck Disease.

Abstract

LncRNA myocardial infarction associated transcript (MIAT) has been shown to be involved in osteoarthritis (OA), but its role in Kashin-Beck Disease (KBD) has rarely been reported. In this study, rats were administered with low selenium and/or T-2 toxin for 4 weeks to establish a KBD animal model. The serum selenium level, TNF-α and IL-1β contents, phosphorylated p65 (p-p65) and MIAT expression were increased in each intervention group. Next, we isolated the primary epiphyseal chondrocytes, and found that selenium treatment reversed the effects of T-2 toxin on chondrocyte injury, p-p65 and MIAT expression. In addition, MIAT overexpression or T-2 toxin treatment led to increased cell death, apoptosis, inflammation, NF-κB-p65 pathway activation and MIAT expression, which was rescued by selenium treatment or MIAT siRNA transfection. Our results suggested that lncRNA MIAT regulated by selenium and T-2 toxin increased the activation of NF-κB-p65, thus being involved in the progress of KBD.

• Authors: Min Shi, Ying He, Ying Zhang, Xiaobo Guo, Jing Lin, Wei Wang, Jinghong Chen
• Journal: Human & experimental toxicology (Hum Exp Toxicol) Vol. 40 Issue 5 Pg. 869-881 (May 2021) ISSN: 1477-0903 [Electronic] England
• PMID: 33233966 (Publication Type: Journal Article, Retracted Publication)

Chemical References

• Interleukin-1beta
• NF-kappa B
• RNA, Long Noncoding
• Tumor Necrosis Factor-alpha
• Selenium
• T-2 Toxin

Topics

• Animals
• Disease Models, Animal
• Humans
• Interleukin-1beta (drug effects)
• Kashin-Beck Disease (chemically induced, genetics, physiopathology)
• Male
• NF-kappa B (drug effects, genetics)
• RNA, Long Noncoding (drug effects)
• Rats
• Rats, Sprague-Dawley
• Selenium (blood, toxicity)
• T-2 Toxin (blood, genetics, toxicity)
• Tumor Necrosis Factor-alpha (drug effects)