RETRACTED: 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. [Formula: see text]

Deoxynivalenol: Emerging Toxic Mechanisms and Control Strategies, Current and Future Perspectives

“…13 The mechanism involved in mycotoxin toxicity includes lncRNA. 11,30 Several studies have found that exposure to aflatoxin B 1 (AFB 1 ) changes the expression of lncRNA and promotes the development of hepatotoxicity and cancer. 31−33 OTA induces the overexpression of lncRNA in renal cell carcinoma and is related to cell death pathways and metabolism.…”

“…Noncoding RNA is a key regulator of toxicological processes and a promising biomarker for the monitoring and prevention of mycotoxin contamination . The mechanism involved in mycotoxin toxicity includes lncRNA. , Several studies have found that exposure to aflatoxin B 1 (AFB 1 ) changes the expression of lncRNA and promotes the development of hepatotoxicity and cancer. − OTA induces the overexpression of lncRNA in renal cell carcinoma and is related to cell death pathways and metabolism . The involvement of lncRNA in the regulation of mycotoxins is expected to become the focus of research because two lncRNAs (XLOC_302848 and XLOC_321638) are potential regulators of Fusarium head blight resistance .…”

Effective protective agents against the organ toxicity of T-2 toxin and corresponding detoxification mechanisms: A narrative review

“… Reversing the effects of T-2 on chondrocyte injury. Shi et al. (2021) Rats Administered with T-2 (200 ng/g BW per day) for 4 weeks under the Se-deficient diet.…”

Combined toxic effects of T-2 toxin and propiconazole on the early life stages of zebrafish (Danio rerio)

“…The increase in leukocyte number and the decrease in bactericidal activity indicate that the T-2 can affect both non-specific cellular and humoral immunity in rainbow trout (Oncorhynchus mykiss) [18]. Ingestion of T-2-contaminated food not only can cause damage to tissues and organs, but also is closely related to degenerative joint diseases, such as Kashin-Beck disease (KBD) [19][20][21]. Propiconazole (PRO) is a triazole fungicide commonly used on corn, wheat, and vegetables worldwide [22].…”