Increased glyoxalase I levels inhibit accumulation of oxidative stress and an advanced glycation end product in mouse mesangial cells cultured in high glucose

The glyoxal-lysine dimer (GOLD), which is a glyoxal (GO)-derived advanced glycation end product (AGE), is produced by the glycation reaction. In this study, we evaluated the effect of GOLD on the oxidative damage and inflammatory response in SV40 MES 13 mesangial cells. GOLD significantly increased the linkage with the V-type immunoglobulin domain of RAGE, a specific receptor of AGE. We found that GOLD treatment increased RAGE expression and reactive oxygen species (ROS) production in mesangial cells. GOLD remarkably regulated the protein and mRNA expression of nuclear factor erythroid 2-related factor 2 (NRF2) and glyoxalase 1 (GLO1). In addition, mitochondrial deterioration and inflammation occurred via GOLD-induced oxidative stress in mesangial cells. GOLD regulated the mitogen-activated protein kinase (MAPK) and the release of proinflammatory cytokines associated with the inflammatory mechanism of mesangial cells. Furthermore, oxidative stress and inflammatory responses triggered by GOLD were suppressed through RAGE inhibition using RAGE siRNA. These results demonstrate that the interaction of GOLD and RAGE plays an important role in the function of mesangial cells.

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Over-production of nitric oxide by oxidative stress-induced activation of the TGF-β1/PI3K/Akt pathway in mesangial cells cultured in high glucose

Acta Pharmacologica Sinica ◽

10.1038/aps.2012.207 ◽

2013 ◽

Vol 34 (4) ◽

pp. 507-514 ◽

Cited By ~ 24

Author(s):

Yun-peng Zhai ◽

Qian Lu ◽

Yao-wu Liu ◽

Qian Cheng ◽

Ya-qin Wei ◽

...

Keyword(s):

Oxidative Stress ◽

Nitric Oxide ◽

High Glucose ◽

Mesangial Cells ◽

Akt Pathway ◽

Tgf Β1 ◽

Cells Cultured

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Mitogen-activated protein kinase cascade is activated in glomeruli of diabetic rats and glomerular mesangial cells cultured under high glucose conditions

Diabetes ◽

10.2337/diabetes.46.5.847 ◽

1997 ◽

Vol 46 (5) ◽

pp. 847-853 ◽

Cited By ~ 39

Author(s):

M. Haneda ◽

S. Araki ◽

M. Togawa ◽

T. Sugimoto ◽

M. Isono ◽

...

Keyword(s):

Protein Kinase ◽

High Glucose ◽

Mesangial Cells ◽

Diabetic Rats ◽

Mitogen Activated Protein Kinase ◽

Glomerular Mesangial Cells ◽

Mitogen Activated Protein ◽

Kinase Cascade ◽

Protein Kinase Cascade ◽

Cells Cultured

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Circ-ACTR2 aggravates the high glucose-induced cell dysfunction of human renal mesangial cells through mediating the miR-205-5p/HMGA2 axis in diabetic nephropathy

Diabetology & Metabolic Syndrome ◽

10.1186/s13098-021-00692-x ◽

2021 ◽

Vol 13 (1) ◽

Author(s):

Jie Yun ◽

Jinyu Ren ◽

Yufei Liu ◽

Lijuan Dai ◽

Liqun Song ◽

...

Keyword(s):

Oxidative Stress ◽

Diabetic Nephropathy ◽

High Glucose ◽

Cell Injury ◽

Mesangial Cells ◽

Protein Detection ◽

Cell Counting ◽

Luciferase Reporter ◽

Enzyme Linked Immunosorbent Assay ◽

Cell Dysfunction

Abstract Background Circular RNAs (circRNAs) have been considered as pivotal biomarkers in Diabetic nephropathy (DN). CircRNA ARP2 actin-related protein 2 homolog (circ-ACTR2) could promote the HG-induced cell injury in DN. However, how circ-ACTR2 acts in DN is still unclear. This study aimed to explore the molecular mechanism of circ-ACTR2 in DN progression, intending to provide support for the diagnostic and therapeutic potentials of circ-ACTR2 in DN. Methods RNA expression analysis was conducted by the quantitative reverse transcription-polymerase chain reaction (qRT-PCR). Cell growth was measured via Cell Counting Kit-8 and EdU assays. Inflammatory response was assessed by Enzyme-linked immunosorbent assay. The protein detection was performed via western blot. Oxidative stress was evaluated by the commercial kits. The molecular interaction was affirmed through dual-luciferase reporter and RNA immunoprecipitation assays. Results Circ-ACTR2 level was upregulated in DN samples and high glucose (HG)-treated human renal mesangial cells (HRMCs). Silencing the circ-ACTR2 expression partly abolished the HG-induced cell proliferation, inflammation and extracellular matrix accumulation and oxidative stress in HRMCs. Circ-ACTR2 was confirmed as a sponge for miR-205-5p. Circ-ACTR2 regulated the effects of HG on HRMCs by targeting miR-205-5p. MiR-205-5p directly targeted high-mobility group AT-hook 2 (HMGA2), and HMGA2 downregulation also protected against cell injury in HG-treated HRMCs. HG-mediated cell dysfunction was repressed by miR-205-5p/HMGA2 axis. Moreover, circ-ACTR2 increased the expression of HMGA2 through the sponge effect on miR-205-5p in HG-treated HRMCs. Conclusion All data have manifested that circ-ACTR2 contributed to the HG-induced DN progression in HRMCs by the mediation of miR-205-5p/HMGA2 axis.

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