Modulation of Nrf2 expression alters high glucose-induced oxidative stress and antioxidant gene expression in mouse mesangial cells

Li, Hang; Wang, Fuxu; Zhang, Lianshan; Cao, Yanping; Liu, Wei; Hao, Jun; Liu, Qingjuan; Duan, Huijun

doi:10.1016/j.cellsig.2011.05.016

Cited by 58 publications

(41 citation statements)

References 35 publications

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“…It has also been found that NFB transcriptional activation requires ROS (69) and NFB is activated in response to HG in endothelial cells (70). Recently, the activation of Nrf-2 in response to the increased ROS induced by HG has been documented and appears to be a negative feedback, protective pathway by inducing an antioxidant response (71). The lack of upregulation of enzymes such as HO-1, a Nrf-2 responsive gene, in Hcb-19 MC in HG is consistent with the absence of ROS generation.…”

Section: Discussionmentioning

confidence: 99%

Thioredoxin-interacting Protein Mediates High Glucose-induced Reactive Oxygen Species Generation by Mitochondria and the NADPH Oxidase, Nox4, in Mesangial Cells

Shah

Xia

Goldberg

et al. 2013

Journal of Biological Chemistry

129

112

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Background: Thioredoxin-interacting protein (TxNIP) is up-regulated by high glucose (HG), inhibits the antioxidant, thioredoxin, and thereby is implicated in oxidative stress. Results: TxNIP deficiency protects mesangial cells from HG-induced oxidative stress and increased collagen by blocking mitochondrial glucose metabolism, NADPH oxidase, and Nox4. Conclusion: TxNIP controls ROS generation by regulating the TCA cycle versus glycolytic glucose flux. Significance: Inhibition of TxNIP is a promising approach to treat glucose toxicity.

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Section: Discussionmentioning

confidence: 99%

Thioredoxin-interacting Protein Mediates High Glucose-induced Reactive Oxygen Species Generation by Mitochondria and the NADPH Oxidase, Nox4, in Mesangial Cells

Shah

Xia

Goldberg

et al. 2013

Journal of Biological Chemistry

129

112

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“…Mouse mesangial cells treated with high glucose demonstrated increased ROS levels, transforming growth factor-b1 (TGF-b1) expression and proliferation (80). Inducing expression of Nrf2 caused a decrease in markers of ROS and oxidantmediated damage in the presence of high glucose.…”

Section: Glomerular Diseasesmentioning

confidence: 99%

“…Inducing expression of Nrf2 caused a decrease in markers of ROS and oxidantmediated damage in the presence of high glucose. Upon Nrf2 induction, increased levels of HO-1 and glutamate cysteine ligase, an enzyme involved in antioxidant glutathione synthesis, were observed (80). Upregulation of Nrf2 may provide an avenue for therapeutics for diabetic kidney disease.…”

Section: Glomerular Diseasesmentioning

confidence: 99%

Heme Oxygenase-1 in Kidney Health and Disease

Lever

Boddu

George

et al. 2016

Antioxidants & Redox Signaling

115

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“…Upon activation, Nrf2 translocates to the nucleus and binds to the antioxidant response element (ARE), which mediates the induction of a spectrum of cytoprotective proteins: the reduced form of nicotinamide adenine dinucleotide phosphate (NADPH):quinone oxidoreductase, heme oxygenase [11], glutathione reductase, superoxide dismutase (SOD) and catalase (CAT) [12]. Impairment of the Nrf2-ARE pathway has been observed in retinal endothelial cells, H9c2 cells, mesangial cells and coronary arterial endothelial cells induced by hyperglycemia, and glucose-induced impairments are prevented by activation of the Nrf2 pathway [13,14,15,16]. However, the role of activation of the Nrf2-ARE pathway in podocyte injury induced by hyperglycemia is not known.…”

Section: Introductionmentioning

confidence: 99%

Activation of the Nrf2-ARE Pathway Attenuates Hyperglycemia-Mediated Injuries in Mouse Podocytes

Wang

Peng

et al. 2014

Cell Physiol Biochem

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Background: Damage to podocytes caused by excessive reactive oxygen species (ROS) contributes to onset and progression of diabetic kidney disease (DKD). Nuclear factor (erythroid-derived 2)-like 2 (Nrf2) is a redox-sensing transcription factor that can induce the expression of antioxidant enzymes. We explored whether activation of Nrf2 pathway attenuated hyperglycemia-induced injuries in mouse podocytes. Methods: Tert-Butylhydroquinone (tBHQ) and small interfering RNAs (siRNAs) were used to regulate Nrf2 expression. Apoptosis and intracellular superoxide anion production were measured by flow cytometry. The activity of the Nrf2 antioxidant pathway was measured by an antioxidant response element (ARE)-driven luciferase reporter gene assay, and Nrf2 expression was assessed by real-time PCR and western blot analyses. Results: Podocytes incubated with high-glucose (HG) medium had higher intracellular superoxide anion and hydrogen peroxide production, higher apoptosis rate, higher bovine serum albumin (BSA) permeability and lower synaptopodin expression compared with podocytes exposed normal glucose (NG) (p<0.05). tBHQ increased the activity of the Nrf2 antioxidant pathway and enhanced nuclear Nrf2 expression, reduced intracellular superoxide anion and hydrogen peroxide production, apoptosis rate and BSA permeability, and restored synaptopodin expression in podocytes exposed to HG (p

show abstract

Modulation of Nrf2 expression alters high glucose-induced oxidative stress and antioxidant gene expression in mouse mesangial cells

Cited by 58 publications

References 35 publications

Thioredoxin-interacting Protein Mediates High Glucose-induced Reactive Oxygen Species Generation by Mitochondria and the NADPH Oxidase, Nox4, in Mesangial Cells

Thioredoxin-interacting Protein Mediates High Glucose-induced Reactive Oxygen Species Generation by Mitochondria and the NADPH Oxidase, Nox4, in Mesangial Cells

Heme Oxygenase-1 in Kidney Health and Disease

Activation of the Nrf2-ARE Pathway Attenuates Hyperglycemia-Mediated Injuries in Mouse Podocytes

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