Ras Activation Modulates Methylglyoxal-Induced Mesangial Cell Apoptosis Through Superoxide Production

Huang, Wei; Tung, Chun Wu; Ho, Cheng; Yang, Jing‐Tang; Chen, Min Li; Chang, Pey‐Jium; Lee, Pei Hsien; Lin, Chun Liang; Wang, Jeng Yi

doi:10.1080/08860220701573509

Cited by 17 publications

(5 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…MG also induces apoptosis of various types of cells [21][22][23][24] and induces oxidative stress, resulting in the generation of ROS 25,26 . Furthermore, administration of MG induces inflammatory responses that include increased expression of interleukin (IL)-1β and tumor necrosis factor-alpha (TNF-α) 27 .…”

Section: Introductionmentioning

confidence: 99%

Methylglyoxal-mediated alteration of gene expression in human endothelial cells

et al. 2011

View full text Add to dashboard Cite

Endothelial dysfunction is an important factor in the development of vascular diseases such as atherosclerosis, hypertension and diabetes. Methylglyoxal (MG) is a highly reactive dicarbonyl metabolite that is an extremely toxic glucose degradation product with strong oxidative activity. MG is involved in the pathogenesis of vascular complications of diabetes. Several studies have reported increased MG levels in pathology models of vascular injury. The present study investigated the genome-wide transcriptional responses of human umbilical vein endothelial cells (HUVECs) exposed to MG by microarray gene expression profiling. As a result, we identified 1,624 genes that were 1.5-fold up-or down-regulated within 12 h of MG treatment. The differentially expressed genes that were dysregulated in many biological processes included inflammatory responses, cell cycle, apoptosis, and cell adhesion. These results demonstrate the MG induced genome-wide alterations in expression profile in human endothelial cells and indicate that MG may cause cytotoxicity and tissue injury in the human endothelium. The data supports the view that MG-stimulated changes in gene expression contribute to the development of vascular disease.

show abstract

Section: Introductionmentioning

confidence: 99%

Methylglyoxal-mediated alteration of gene expression in human endothelial cells

et al. 2011

View full text Add to dashboard Cite

show abstract

“…20 The cytotoxicity of MG to tissues or cells results to trigger apoptosis. 21 Therefore, mitochondria are important targets for studying the effects in the MG-mediated apoptotic process.…”

Section: Introductionmentioning

confidence: 99%

Phycocyanin prevents methylglyoxal-induced mitochondrial-dependent apoptosis in INS-1 cells by Nrf2

et al. 2016

View full text Add to dashboard Cite

Methylglyoxal (MG) is a reactive dicarbonyl compound, whose abnormal accumulation in diabetic patients exerts deleterious effects on cells and tissues. The β-cell is the main target cell of Type 2 diabetes, and its insulin secretion injury and cell apoptosis can be due to mitochondrial dysfunction. Previous studies have demonstrated MG induced β-cell apoptosis. However, little is known about the effect of MG on β-cell mitochondrial dysfunction. Phycocyanin (PC) has been demonstrated to possess various biological activities including the effects on diabetic models in vivo. The aim of this study was to determine the protective effect of PC against methylglyoxal (MG)-induced dysfunction in pancreatic β-cell INS-1 and also the mechanism. We demonstrated that MG induced mitochondrial dysfunction by the decline in ATP levels, and the increase of the level of intracellular reactive oxygen species (ROS). Furthermore, MG released cytochrome c and apoptosis-inducing factor (AIF) from the mitochondrion, induced changes in the expression of Bcl-2 family members, activated caspases and increased PARP cleavage. Interestingly, PC activated nuclear erythroid-related factor 2 (Nrf2), and Nrf2 activation as well as antioxidant enzymes HO-1 and glyoxalase 1 (Glo-1) were confirmed to be involved in the mechanisms underlying the protection of PC by RNA interference. Altogether, these results demonstrated that PC prevented mitochondrial-dependent apoptosis in MG-induced INS-1 cells and the effect was associated with Nrf2 activation.

show abstract

“…MGO is associated with the formation of acellular capillaries and a loss of pericytes in diabetic rats [15,16]. Cytotoxicity induced by MGO has already been reported in various cells (rat Schwann cells, human vascular endothelial cells, rat mesangial cell and bovine retinal pericytes) [17][18][19][20]. In this study, we show that the exposure of retinas to MGO leads to an alteration of the BRB.…”

Section: Discussionmentioning

confidence: 72%

Methylglyoxal induces hyperpermeability of the blood–retinal barrier via the loss of tight junction proteins and the activation of matrix metalloproteinases

Kim

Lee

et al. 2012

Graefes Arch Clin Exp Ophthalmol

View full text Add to dashboard Cite

show abstract

Ras Activation Modulates Methylglyoxal-Induced Mesangial Cell Apoptosis Through Superoxide Production

Abstract: This study has shown that methylglyoxal increased Ras modulation of superoxide-mediated P38 activation and c-Jun activation, which resulted in increased apoptosis.

Cited by 17 publications

References 17 publications

Methylglyoxal-mediated alteration of gene expression in human endothelial cells

Methylglyoxal-mediated alteration of gene expression in human endothelial cells

Phycocyanin prevents methylglyoxal-induced mitochondrial-dependent apoptosis in INS-1 cells by Nrf2

Methylglyoxal induces hyperpermeability of the blood–retinal barrier via the loss of tight junction proteins and the activation of matrix metalloproteinases

Contact Info

Product

Resources

About