scholarly journals MicroRNA-223 ameliorates alcoholic liver injury by inhibiting the IL-6–p47phox–oxidative stress pathway in neutrophils

Gut ◽  
2016 ◽  
Vol 66 (4) ◽  
pp. 705-715 ◽  
Author(s):  
Man Li ◽  
Yong He ◽  
Zhou Zhou ◽  
Teresa Ramirez ◽  
Yueqiu Gao ◽  
...  
2021 ◽  
Author(s):  
pei shengfei ◽  
luming yang ◽  
lin wang ◽  
xuelei gao ◽  
yu guo ◽  
...  

Abstract BackgroundAnti-tuberculosis drug-induced liver injury (ADLI) limits the treatment of tuberculosis. The mechanisms underlying ADLI are unclear and there are no effective preventative measures to avoid this complication. MethodsIn this stuy, the protein contents of EZH2, Nrf2, NQO1 and HO-1 were detected by ELISA kit, while those of EZH2 and Nrf2 were determined by Western blot. The Chip experiment was used to detect the level of H3K27me3 in the Nrf2 promoter region.The liver were analyzed histopathologically in vivo using hematoxylin and eosin staining.ResultsHere we developed a murine model of ADLI that recapitulates liver injury in the human disease. Using this model, we investigated the potential involvement of the enhancer of zeste homolog 2 methyltransferase (EZH2), a histone methyltransferase which inhibits the transcriptional activation of the Nrf2-ARE oxidative stress pathway. Compared to controls, mice livers with ADLI showed decreased expression of EZH2 together with reduced H3K27me3 marks in the Nrf2 promoter. This was accompanied by increased expression of Nrf2 and its target genes NQO1 and HO-1. Liver injury in the mice with ADLI could be alleviated to an extent by in vivo delivery of siRNAs targeting EZH2, which further downregulated EZH2 expression and H3K27me3 levels in the Nrf2 promoter along with accompanying increases in Nrf2, NQO1 and HO-1 expression. ConclusionsTherefore, inhibiting EZH2 likely reduced liver damage in ADLI by enhancing this key anti-oxidative stress pathway. Our results establish a role for EZH2 in a mouse model of ADLI and furthermore provides valuable mechanistic insights into the development of ADLI pathology.


2009 ◽  
Vol 23 (2) ◽  
pp. 102-111 ◽  
Author(s):  
Arun K. Tiwari ◽  
Pushplata Prasad ◽  
Thelma B.K. ◽  
K.M. Prasanna Kumar ◽  
A.C. Ammini ◽  
...  

2020 ◽  
Author(s):  
Jianfeng Li ◽  
Shaoyu Hu ◽  
Song Hao ◽  
Shengjia Huang ◽  
Yi Qin ◽  
...  

Abstract Background The role of gene and pathway in recurrence of Ewing sarcoma (ES) was not clear. Thus, we investigated the biological role and underlying mechanism of gene and pathway in recurrence of ES. Methods Data sets of patients with ES were collected from the GEO database. We used dataset GSE63155 and GSE63156 to construct co-expression networks by weighted gene co-expression network analysis (WGCNA). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed by Database for Annotation, Visualization and Integrated Discovery (DAVID). Results We can find that genes with significant interactions in the genes of the recurrence group include SRSF11, TRIM39, SOCS3,NUPL2,COPS5. They work primarily through the oxidative stress pathway. Conclusion Through our research, for the first time found that ES by SRSF11 TRIM39, SOCS3, NUPL2, COPS5 interaction, activation of phosphorylation of bone and oxidative stress is affecting tumor recurrence.


Autophagy ◽  
2019 ◽  
Vol 16 (5) ◽  
pp. 917-931 ◽  
Author(s):  
Zhiqiang Deng ◽  
Junghyun Lim ◽  
Qian Wang ◽  
Kerry Purtell ◽  
Shuai Wu ◽  
...  

2019 ◽  
Vol 30 (12) ◽  
pp. 1365-1375
Author(s):  
Zhenzhen Zhang ◽  
Duo Jiang ◽  
Chi Wang ◽  
Mark Garzotto ◽  
Ryan Kopp ◽  
...  

Sign in / Sign up

Export Citation Format

Share Document