Methylglyoxal‐induced Fibronectin gene expression through Ras‐mediated NADPH oxidase activation in renal mesangial cells

Ho, Cheng; Lee, Pei Hsien; Huang, Wei; Hsu, Yu-Ting; Lin, Chun Liang; Wang, Jeng Yi

doi:10.1111/j.1440-1797.2007.00809.x

Cited by 30 publications

(13 citation statements)

References 32 publications

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“…syndecans). Several factors in the diabetic milieu including a highly reactive dicarbonyl compound methylglyoxal [58], superoxide [59], nitric oxide [60], activated Ras (GTP-binding proteins of small-molecular-weight) [59], and increased aldose reductase activity [61,62] have been reported to increase fibronectin expression in renal mesangial and proximal tubular cells. Renal fibronectin accumulation has been identified in several animal models of diabetic nephropathy, and has been found amenable to correction by pharmacological agents counteracting expansion of the mesangial extracellular matrix [9,62].…”

Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model

Shevalye¹,

Stavniichuk²,

Xu³

et al. 2010

Biochemical Pharmacology

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Evidence for the important role for poly(ADP-ribose) polymerase (PARP) in the pathogenesis of diabetic nephropathy is emerging. We previously reported that PARP inhibitors counteract early Type 1 diabetic nephropathy. This study evaluated the role for PARP in kidney disease in long-term Type 1 diabetes. Control and streptozotocin-diabetic rats were maintained with or without treatment with the PARP inhibitor 10-(4-methyl-piperazin-1-ylmethyl)-2H-7-oxa-1,2-diaza-benzo[de] anthracen-3-one (GPI-15,427, Eisai Inc.), 30 mg kg−1d−1, for 26 weeks after first 2 weeks without treatment. PARP activity in the renal cortex was assessed by Western blot analysis of poly(ADP-ribosyl)ated proteins. Urinary albumin, isoprostane, and 8-hydroxy-2′-deoxyguanosine excretion, and renal concentrations of transforming growth factor-β1, vascular endothelial growth factor, soluble intercellular adhesion molecule-1, fibronectin, and nitrotyrosine were evaluated by ELISA, and urinary creatinine and renal lipid peroxidation products by colorimetric assays. PARP inhibition counteracted diabetes-associated increase in renal cortex poly(ADP-ribosyl)ated protein level. Urinary albumin, isoprostane, and 8-hydroxy-2′-deoxyguanosine excretions and urinary albumin/creatinine ratio were increased in diabetic rats, and all these changes were at least partially prevented by GPI-15,427 treatment. PARP inhibition counteracted diabetes-induced renal transforming growth factor-β1, vascular endothelial growth factor, and fibronectin, but not soluble intercellular adhesion molecule-1 and nitrotyrosine, accumulations. Lipid peroxidation product concentrations were indistinguishable among control and diabetic rats maintained with or without GPI-15,427 treatment. In conclusion, PARP activation plays an important role in kidney disease in long-term diabetes. These findings provide rationale for development and further studies of PARP inhibitors and PARP inhibitor-containing combination therapies, for prevention and treatment of diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model

Shevalye¹,

Stavniichuk²,

Xu³

et al. 2010

Biochemical Pharmacology

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“…Scavenging ROS reversed TGF-b and fibronectin level [48]. Particularly, TGF-b is important in accumulation of ECM components and the development of adhesion and subsequent fibrosis in endometriosis.…”

Section: Fibronectinmentioning

confidence: 98%

New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal

Kajihara

Yamada

Kanayama

et al. 2010

Gynecological Endocrinology

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“…Furthermore, methylglyoxal can activate Nox in certain cells to increase superoxide, leading to induction of specific matrix molecules including fibronectin (74,120). Methylglyoxal accumulates after radiation-induced redox stress, and glutathione is required for its metabolism to lactate via Slactoylglutathione and glyoxalase I. Ionizing radiation induces glyoxalases I and II (230).…”

Section: B Cd47-dependent Regulation Of Redox Metabolites In Irradiamentioning

confidence: 99%

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

Roberts

Kaur

Isenberg

2017

Antioxidants & Redox Signaling

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Significance: In contrast to structural elements of the extracellular matrix, matricellular proteins appear transiently during development and injury responses, but their sustained expression can contribute to chronic disease. Through interactions with other matrix components and specific cell surface receptors, matricellular proteins regulate multiple signaling pathways, including those mediated by reactive oxygen and nitrogen species and H 2 S. Dysregulation of matricellular proteins contributes to the pathogenesis of vascular diseases and cancer. Defining the molecular mechanisms and receptors involved is revealing new therapeutic opportunities. Recent Advances: Thrombospondin-1 (TSP1) regulates NO, H 2 S, and superoxide production and signaling in several cell types. The TSP1 receptor CD47 plays a central role in inhibition of NO signaling, but other TSP1 receptors also modulate redox signaling. The matricellular protein CCN1 engages some of the same receptors to regulate redox signaling, and ADAMTS1 regulates NO signaling in Marfan syndrome. In addition to mediating matricellular protein signaling, redox signaling is emerging as an important pathway that controls the expression of several matricellular proteins. Critical Issues: Redox signaling remains unexplored for many matricellular proteins. Their interactions with multiple cellular receptors remains an obstacle to defining signaling mechanisms, but improved transgenic models could overcome this barrier. Future Directions: Therapeutics targeting the TSP1 receptor CD47 may have beneficial effects for treating cardiovascular disease and cancer and have recently entered clinical trials. Biomarkers are needed to assess their effects on redox signaling in patients and to evaluate how these contribute to their therapeutic efficacy and potential side effects. Antioxid. Redox Signal. 27, 874-911.

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Methylglyoxal‐induced Fibronectin gene expression through Ras‐mediated NADPH oxidase activation in renal mesangial cells

Abstract: Induction of superxoide by Ras via p38 pathway activates fibrotic gene transcription of mesangial cells. Reduction of oxidative stress by scavenging superoxide may offer an alternative strategy for controlling MGO-induced renal fibrosis.

Cited by 30 publications

References 32 publications

Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model

Poly(ADP-ribose) polymerase (PARP) inhibition counteracts multiple manifestations of kidney disease in long-term streptozotocin-diabetic rat model

New insights into the pathophysiology of endometriosis: from chronic inflammation to danger signal

Regulation of Cellular Redox Signaling by Matricellular Proteins in Vascular Biology, Immunology, and Cancer

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