Downregulation of miR-31 in Diabetic Nephropathy and its Relationship with Inflammation

Rovira‐Llopis, Susana; Escribano-López, Irene; Díaz-Morales, Noelia; Iannantuoni, Francesca; López‐Domènech, Sandra; Andújar, Isabel; Jover, A; Pantoja, Jonay; Pallardó, Luís; Bañuls, Celia; Víctor, Víctor M.

doi:10.1159/000494485

Cited by 49 publications

(34 citation statements)

References 31 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Increasing evidences have demonstrated that miRNAs play a key role in the pathogenesis of DN [29,30]. For example, Wang et al [31] found that miR-424 was down-regulated in renal tissues of DN rats and up-regulation of miR-424 obviously improved the symptoms in DN rat models by targeting Rictor.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

Ren

Chen

et al. 2020

Bioscience Reports

View full text Add to dashboard Cite

Hyperglycemia-induced renal tubular cell injury is thought to play a critical role in the pathogenesis of diabetic nephropathy (DN). However, the role of miRNAs in renal tubular cell injury remains to be fully elucidated. The aim of the present study was to investigate the role and mechanisms of miRNAs protecting against high glucose (HG)-induced apoptosis and inflammation in renal tubular cells. First, we analyzed microRNA (miRNA) expression profiles in kidney tissues from DN patients using miRNA microarray. It was observed that miRNA-140-5p (miR-140-5p) was significantly down-regulated in kidney tissues from patients with DN. An inverse correlation between miR-140-5p expression levels with serum proteinuria was observed in DN patients, suggesting miR-140-5p may be involved in the progression of DN. HG-induced injury in HK-2 cells was used to explore the potential role of miR-140-5p in DN. We found that miR-140-5p overexpression improved HG-induced cell injury, as evidenced by the enhancement of cell viability, and inhibition of the activity of caspase-3 and reactive oxygen species (ROS) generation. It was also observed that up-regulation of miR-140-5p suppressed HG induced the expressions of pro-inflammatory cytokines, such as tumor necrosis factor-α (TNF-α), interleukin (IL)-1β and IL-6 in HK-2 cells. In addition, TLR4, one of the upstream molecules of NF-κB signaling pathway, was found to be a direct target of miR-140-5p in the HK-2. Moreover, the HG-induced activation of NF-κB signaling pathway was inhibited by miR-140-5p overexpression. These results indicated that miR-140-5p protected HK-2 cells against HG-induced injury through blocking the TLR4/NF-κB pathway, and miR-140-5p may be considered as a potential prognostic biomarker and therapeutic target in the treatment of DN.

show abstract

Section: Discussionmentioning

confidence: 99%

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

Ren

Chen

et al. 2020

Bioscience Reports

View full text Add to dashboard Cite

show abstract

“…CircRNAs generally exhibit regulatory functions on gene expression through acting as microRNA sponge . miR‐31 are reported to present pro‐inflammatory or anti‐inflammatory activities under different condition . Besides, earlier literature reported that miR‐31 presented anti‐inflammatory activity on lung cystic fibrosis and its expression was reduced in lung cystic fibrosis airways .…”

Section: Discussionmentioning

confidence: 99%

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

2019

View full text Add to dashboard Cite

Background Some circular RNAs (circRNAs) are reported to attend to the pathogenesis of pneumonia. This study tested the impact of circRNA ankyrin repeat domain 36 (circANKRD36) on human embryonic lung fibroblast MRC‐5 cell injury irritated by lipopolysaccharide (LPS). Methods After LPS irritation, viability, apoptosis, ROS, protein, and cytokines, along with circANKRD36 were tested by CCK‐8, Annexin V‐FITC, DCFH‐DA, and ELISA or Western blot. si‐circANKRD36 and microRNA‐31‐3p/5p (miR‐31‐3p/5p) inhibitor were applied to silence circANKRD36 and miR‐31‐3p/5p. miR‐31‐3p/5p mimic was utilized to upregulate miR‐31‐3p/5p. RT‐qPCR was used to detect miRNAs. The relationship between miRNAs and MyD88 or IL‐34 was analyzed by luciferase activity reporter assay. Results LPS aroused a decrease in viability, increases in apoptosis, ROS, and IL‐6, IL‐8, and TNF‐α, along with circANKRD36, and activation of NF‐κB pathway. Silencing circANKRD36 weakened the above‐mentioned influences of LPS. Moreover, silencing circANKRD36 hoisted miR‐31‐3p expression. Silencing miR‐31‐3p mitigated the impacts of circANKRD36 silence on LPS‐irritated MRC‐5 cells. Besides, MyD88 was a downstream target of miR‐31‐3p, and 3′UTR of IL‐34 mRNA was targeted by miR‐31‐5p. LPS induced the accumulation of MyD88. Silencing MyD88 was constructive to maintain cell viability, retard apoptosis and inhibit adverse oxidation and inflammation. Conclusion This research verified that silencing circANKRD36 could weaken LPS‐irritated MRC‐5 cell injury via regulating miR‐31/MyD88‐mediated repression of NF‐κB pathway.

show abstract

“…However, this miR was not among the top 10 miRs regulated in human renal cells or urines from patients. This indicated that a species‐specific miR‐analysis seems to be important as there might be differences in miR‐expression in humans and rats …”

Section: Discussionmentioning

confidence: 99%

Identification of cell and disease specific microRNAs in glomerular pathologies

Müller-Deile

Dannenberg

Liu

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

MicroRNAs (miRs) are small non‐coding RNAs that regulate gene expression in physiological processes as well as in diseases. Currently miRs are already used to find novel mechanisms involved in diseases and in the future, they might serve as diagnostic markers. To identify miRs that play a role in glomerular diseases urinary miR‐screenings are a frequently used tool. However, miRs that are detected in the urine might simply be filtered from the blood stream and could have been produced anywhere in the body, so they might be completely unrelated to the diseases. We performed a combined miR‐screening in pooled urine samples from patients with different glomerular diseases as well as in cultured human podocytes, human mesangial cells, human glomerular endothelial cells and human tubular cells. The miR‐screening in renal cells was done in untreated conditions and after stimulation with TGF‐β. A merge of the detected regulated miRs led us to identify disease‐specific, cell type‐specific and cell stress‐induced miRs. Most miRs were down‐regulated following the stimulation with TGF‐β in all cell types. Up‐regulation of miRs after TGF‐β was cell type‐specific for most miRs. Furthermore, urinary miRs from patients with different glomerular diseases could be assigned to the different renal cell types. Most miRs were specifically regulated in one disease. Only miR‐155 was up‐regulated in all disease urines compared to control and therefore seems to be rather unspecific. In conclusion, a combined urinary and cell miR‐screening can improve the interpretation of screening results. These data are useful to identify novel miRs potentially involved in glomerular diseases.

show abstract

Downregulation of miR-31 in Diabetic Nephropathy and its Relationship with Inflammation

Cited by 49 publications

References 31 publications

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

MicroRNA-140-5p ameliorates the high glucose-induced apoptosis and inflammation through suppressing TLR4/NF-κB signaling pathway in human renal tubular epithelial cells

Retracted: Circular RNA ANKRD36 attends to lipopolysaccharide‐aroused MRC‐5 cell injury via regulating microRNA‐31‐3p

Identification of cell and disease specific microRNAs in glomerular pathologies

Contact Info

Product

Resources

About