MicroRNA-16 is putatively involved in the NF-κB pathway regulation in ulcerative colitis through adenosine A2a receptor (A2aAR) mRNA targeting

@article{Tian2016MicroRNA16IP,
  title={MicroRNA-16 is putatively involved in the NF-$\kappa$B pathway regulation in ulcerative colitis through adenosine A2a receptor (A2aAR) mRNA targeting},
  author={Ting Tian and Yu Zhou and Xiao Feng and Shicai Ye and Hao Wang and Weiyun Wu and Wen-kai Tan and Cai-yuan Yu and Juxiang Hu and Rong Zheng and Zonghao Chen and Xinyu Pei and Hesheng Luo},
  journal={Scientific Reports},
  year={2016},
  volume={6}
}
MicroRNAs (miRNAs) act as important post-transcriptional regulators of gene expression by targeting the 3′-untranslated region of their target genes. Altered expression of miR-16 is reported in human ulcerative colitis (UC), but its role in the development of the disease remains unclear. Adenosine through adenosine A2a receptor (A2aAR) could inhibit nuclear factor-kappaB (NF-κB) signaling pathway in inflammation. Here we identified overexpression of miR-16 and down-regulation of A2aAR in the… 
Downregulation of miR-2143 p May Contribute to Pathogenesis of Ulcerative Colitis via Targeting STAT 6
TLDR
The results of the present study indicate that miR-214-3p and STAT6 axis may be a novel therapeutic target for intestinal inflammation of patients with active UC.
Downregulation of miR-214-3p May Contribute to Pathogenesis of Ulcerative Colitis via Targeting STAT6
TLDR
The results of the present study indicate that miR-214-3p and STAT6 axis may be a novel therapeutic target for intestinal inflammation of patients with active UC.
Upregulated gga-miR-16-5p Inhibits the Proliferation Cycle and Promotes the Apoptosis of MG-Infected DF-1 Cells by Repressing PIK3R1-Mediated the PI3K/Akt/NF-κB Pathway to Exert Anti-Inflammatory Effect
TLDR
Upregulated gga-miR-16-5p could decrease multiplication, cycle progression, and increase apoptosis of MG-infected DF-1 cells, at least partly through directly targeting PIK3R1 and inhibiting PI3K/Akt/NF-κB pathway to exert an anti-inflammatory effect.
Inhibition of miR-378a-3p by Inflammation Enhances IL-33 Levels: A Novel Mechanism of Alarmin Modulation in Ulcerative Colitis
TLDR
A regulatory mechanism of IL-33 expression exerted by miR-378a-3p in an inflammatory environment is proposed, contributing to the understanding of UC pathogenesis.
IL-21 mediates microRNA-423-5p /claudin-5 signal pathway and intestinal barrier function in inflammatory bowel disease
TLDR
It is described that miR-423-5p could be involved in IL-21/ claudin-5 pathway by regulating NF-κB/MAPKs/JNK signaling pathway, which may provide a new therapeutic target for IBD.
The role of microRNA-16 in the pathogenesis of autoimmune diseases: A comprehensive review.
hsa-miR-3177-5p and hsa-miR-3178 Inhibit 5-HT1A Expression by Binding the 3′-UTR Region in vitro
TLDR
Hsa-miR-3177-5p and hsa- miR- 3178 had significant inhibitory effects on expression of the HTR1A gene and 5-HT1A receptor and may directly participate in the development of neuropsychiatric diseases.
Downregulation of miR-16 protects H9c2(2-1) cells against hypoxia/reoxygenation damage by targeting CIAPIN1 and regulating the NF-κB pathway
TLDR
The present study illustrates that downregulation of miR-16 may protect against H/R-induced injury partially by targeting CIAPIN1 and the NF-κB signaling pathway.
The crucial role of non-coding RNAs in the pathophysiology of inflammatory bowel disease.
Circulating exosomal miR-21 mediates HUVEC proliferation and migration through PTEN/PI3K/AKT in Crohn's disease.
TLDR
Circulating exosomal miR-21 mediates HUVEC proliferation and migration through PTEN/PI3K/AKT in CD and may be a new biomarker or therapeutic target for the treatment of vascular abnormalities in CD.
...
...

References

SHOWING 1-10 OF 45 REFERENCES
Up-Regulation of microRNA-126 May Contribute to Pathogenesis of Ulcerative Colitis via Regulating NF-kappaB Inhibitor IκBα
Background MicroRNAs (miRNAs) are important post-transcriptional regulators. Altered expression of miRNAs has recently demonstrated association with human ulcerative colitis (UC). In this study, we
Adenosine 2B Receptor Expression Is Post-transcriptionally Regulated by MicroRNA
TLDR
It is demonstrated that TNF-α-induced A2BAR expression in colonic epithelial cells is post-transcriptionally regulated by miR27b and miR128a and show that miR 27b influences A 2Bar expression in murine colitis.
Role of miR-19a targeting TNF-α in mediating ulcerative colitis
TLDR
This study determines the levels of miR-19a and TNF-α in both DSS-induced experimental murine colitis and human UC and demonstrates that miR -19a might directly regulate TNF -α, and indicates that the findings may provide new insight in the clinical treatment of UC.
Adenosine A2A Receptor Upregulation in Human PMNs Is Controlled by miRNA-214, miRNA-15, and miRNA-16
TLDR
Results indicate that individual miRNA profiles gain important influence on A2AR expression regulation in PMNs upon stimulation, and determination of miRNA expression levels may help to identify patients with an increased risk for severe inflammation.
Dual TNF-α/IL-12p40 Interference as a Strategy to Protect Against Colitis Based on miR-16 Precursors With Macrophage Targeting Vectors.
TLDR
Results show that specific upregulation of miR-16 level in colonic macrophages significantly reduces TNF-α and IL-12p40 expression, which could suppress the associated mucosal inflammation and ultimately result in the relief of colitic symptoms.
Distinct Roles of Heterogeneous Nuclear Ribonuclear Protein K and microRNA-16 in Cyclooxygenase-2 RNA Stability Induced by S100b, a Ligand of the Receptor for Advanced Glycation End Products*♦
TLDR
The new results demonstrate that diabetic stimuli can efficiently stabilize inflammatory genes via opposing actions of key RNA-binding proteins and miRs, further supporting the inhibitory effects of miR-16.
MicroRNAs are differentially expressed in ulcerative colitis and alter expression of macrophage inflammatory peptide-2 alpha.
TLDR
These findings expand the known roles of miRNAs, indicating that tissues from patients with UC, and possibly other chronic inflammatory diseases, have altered miRNA expression patterns and demonstrate that mi RNAs regulate colonic epithelial cell-derived chemokine expression.
MicroRNA-16 suppresses the activation of inflammatory macrophages in atherosclerosis by targeting PDCD4
TLDR
The data demonstrate that the targeting of PDCD4 by miR-16 may suppress the activation of inflammatory macrophages though mitogen-activated protein kinase (MAPK) and NF-κB signaling in atherosclerosis; thus, PD CD4 may prove to be a potential therapeutic target in the treatment of Atherosclerosis.
Nuclear factor-kappa B in intestinal protection and destruction
TLDR
Nuclear factor-kappa B has multiple, often opposing functions in the intestine, whereas proinflammatory and cell survival functions of NF-κB in macrophages and T cells govern chronic intestinal inflammation.
...
...