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.
Background and Aim. Redox equilibria are critical for life, but the biomarkers of redox status are currently unavailable. Gamma-glutamyltransferase (GGT) is an essential factor for modulating redox equilibrium through glutathione. In clinical practice, increased circulating GGT activity is used as a hepatobiliary disease biomarker. However, increased circulating GGT activities have also been observed in cancers, heart disease, diabetes, hyperuricemia, inflammation, renal insufficiency, and other diseases, explained by its role in maintaining redox equilibrium inside and outside cells. Previous studies on GGT were mainly limited to one type of disease at one time. In the current study, we systematically compared the GGT levels in 44 different human diseases to test if it could serve as a redox status biomarker in blood circulation. Methods. The clinical GGT data from 168,858 patients with 44 diseases and 132,357 healthy control in the clinical laboratory of our hospital over the past five years were retrieved. All data were analyzed with SPSS, RStudio V.1.3.1073, and python libraries 3.8. Results. Thirty-eight out of 44 diseases had significantly increased ( p < 0.001 ) circulating GGT activities, whereas gastric cancer, anemia, renal cyst, cervical cancer, preeclampsia, and knee-joint degenerative diseases had significantly decreased ( p < 0.001 ) GGT activities compared to the healthy control. ROC analyses showed that GGT was an excellent biomarker for liver cancer ( AUC = 0.86 ), pancreatitis ( AUC = 0.84 ), or hepatic encephalopathy ( AUC = 0.80 ). All pancreas-related diseases had more than 8-fold increases in GGT activity span than the healthy control, while pancreatic cancer had a 12-fold increase (1021 U/L vs. 82 U/L). The knee-joint degenerative disease had the lowest median and narrowest GGT activity range (63 U/L). Furthermore, most diseases’ lowest to highest GGT activities were beyond the healthy control in both directions. Conclusions. Thirty-eight out of 44 diseases were in overall oxidative states defined by the increased GGT median values. In contrast, knee-joint degenerative disease, gastric cancer, anemia, renal cyst, cervical cancer, and preeclampsia were in overall antioxidative states. Moreover, most diseases swing between oxidative and antioxidative states, evidenced by the increased lowest to highest GGT activity ranges than the healthy control. Liver- and pancreas-related abnormalities were responsible for significantly increased GGT activities. Our overall results suggested that circulating GGT was a redox status biomarker.
Background C‐Jun N‐terminal kinase pathway‐associated phosphatase (JKAP) modulates the T cell receptor and mitogen‐activated protein kinase pathway‐mediated autoimmunity, thus participating in the pathogenesis of autoimmune diseases. This study aimed to explore the clinical implication of JKAP in inflammatory bowel disease (IBD) children. Methods C‐Jun N‐terminal kinase pathway‐associated phosphatase, tumor necrosis factor‐α (TNF‐α), interleukin‐23, interferon‐γ (T‐helper 1 secreted cytokine), and interleukin‐17A (T‐helper 17 secreted cytokine) in serum samples from 140 IBD children (including 60 Crohn's disease (CD) children and 80 ulcerative colitis (UC) children) were detected by ELISA. Meanwhile, JKAP from serum samples of 10 healthy controls (HCs) was also detected by ELISA. Results C‐Jun N‐terminal kinase pathway‐associated phosphatase was reduced in CD children (median (interquartile range (IQR)): 51.6 (36.8–69.5) pg/ml) and UC children (median (IQR): 57.5 (43.4–78.5) pg/ml) compared with HCs (median (IQR): 101.8 (70.0–143.2) pg/ml) (both p < 0.05). In CD children, JKAP was negatively correlated with C‐reactive protein (CRP) ( p = 0.016) and erythrocyte sedimentation rate (ESR) ( p = 0.029); while in UC children, JKAP was also negatively correlated with CRP ( p = 0.006) and ESR ( p = 0.022). Regarding the correlation of JKAP with disease activity, it presented negative correlations with PCDAI ( p = 0.001) and PUCAI ( p = 0.002). Besides, JKAP was negatively related to TNF‐α (both p < 0.05) but not interleukin‐23 (both p >0.05) in CD and UC children. Additionally, JKAP was not correlated with interferon‐γ in CD or UC children (both p >0.05), while negatively correlated with interleukin‐17A in CD and UC children (both p < 0.05). Conclusion C‐Jun N‐terminal kinase pathway‐associated phosphatase shows low expression and negative correlations with inflammation, disease activity, and T‐helper 17 cells in IBD children.
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