Retracted: Long noncoding RNA Mirt2 prohibits lipopolysaccharide‐evoked HK‐2 cell injury via modulation of microRNA‐126

Abstract

Long noncoding RNA myocardial infarction‐associated transcript 2 (lncRNA Mirt2) is a burgeoning lncRNA, its anti‐inflammatory capacity has been testified. Nonetheless, the functions of Mirt2 in immunoglobulin A nephropathy are unexplored. We tried to impart the influences of Mirt2 in lipopolysaccharide (LPS)‐evoked HK‐2 cells damage. HK‐2 cells were manipulated with 10 ng/ml LPS, next cell viability, apoptosis, reactive oxygen species (ROS) generation, pro‐inflammatory factors and Mirt2 expression were evaluated. After pc‐Mirt2 vector transfection, the aforementioned trials were performed. Meanwhile, real‐time quantitative polymerase chain reaction (PCR) experiment was used to detect miR‐126 expression. Subsequently, functions of miR‐126 in LPS‐treated HK‐2 cells were further delved after transfection with miR‐126 mimic. Western blot was used to evaluate NF‐κB pathway. The data showed that LPS invoked HK‐2 cells inflammatory damage via the suppression of cell viability and the acceleration of apoptosis, ROS level, and IL‐1β and IL‐6 secretion. LPS inhibited Mirt2 expression and overexpression of Mirt2 mitigated LPS‐caused inflammatory damage in HK‐2 cells. Additionally, overexpression of Mirt2 repressed miR‐126 expression in LPS‐stimulated cells. Meanwhile the anti‐inflammatory effect of Mirt2 was inverted by upregulating miR‐126 expression. Besides, overexpressed Mirt2 retarded LPS‐activated NF‐κB pathway via repressing miR‐126. The research certified the anti‐inflammatory impacts of Mirt2 on LPS‐impaired HK‐2 cells.

RETRACTED ARTICLE: The myocardial infarction-associated transcript 2 inhibits lipid accumulation and promotes cholesterol efflux in oxidized low-density lipoprotein-induced THP-1-derived macrophages via inhibiting mitogen-activated protein kinase signaling and activating the nuclear factor erythroid-related factor 2 signaling pathway

“…Nuclear factor erythroid-related factor 2 (NRF2) is a redox-sensitive transcription factor that prevents oxidative stress by regulating cytoprotective genes, including NAD(P)H quinone dehydrogenase 1 (NQO1), heme oxygenase 1 (HO-1) and glutamate-cysteine ligase [ 14 ]. It is worth noting that it is reported that after feeding a high-fat diet, NRF2 inhibits lipid accumulation and oxidative stress in the liver tissue of mice by inhibiting lipogenesis and cholesterol production signaling pathways [ 15 ].…”

lncRNA Mirt2 upregulates miR‐1246 through methylation to suppress LPS‐induced lung cell apoptosis

“…Interestingly, a recent study reported that LPS treatment increases Mirt2 expression in macrophages through interactions with p38‐Stat1 and interferon‐Stat1 pathways, and identifies lncRNA Mirt2 as a negative feedback regulator of excessive inflammation. 13 Moreover, Bai et al 18 indicated that LPS suppresses Mirt2 expression and overexpression of Mirt2 mitigates LPS‐induced inflammatory damages in HK‐2 cells. Similarly, Li et al 19 found that lncRNA Mirt2 level is upregulated in LPS‐stimulated PC12 cells and serum samples derived from spinal cord injury patients, and overexpression of lncRNA Mirt2 protects PC12 cells from LPS‐induced injuries.…”

The impact and role of identified long noncoding RNAs in nonalcoholic fatty liver disease: A narrative review

“…Mirt2, termed as myocardial infarction‐associated transcript 2, is a newfound lncRNA with the activity of anti‐inflammatory. 57 Mirt2 decreased in the livers of obese mice, revealing that mirt2 was involved in NAFLD. 58 Liver‐specific mirt2 overexpression improved hepatic glucose tolerance and IR, and alleviated lipid deposition in HFD mice; meanwhile, upregulation of mirt2 improved liver function in obese mice.…”

“…Mirt2, termed as myocardial infarction‐associated transcript 2, is a newfound lncRNA with the activity of anti‐inflammatory 57 . Mirt2 decreased in the livers of obese mice, revealing that mirt2 was involved in NAFLD 58 .…”