High glucose induced endothelial cell reactive oxygen species via OGG1/PKC/NADPH oxidase pathway

Xie, Xiangrong; Chen, Yan; Liu, Jichun; Zhang, Wenbo; Zhang, Xuan; Zha, Lin-Tao; Liu, Wenjie; Ling, Yang; Li, Shu; Tang, Shengxing

doi:10.1016/j.lfs.2020.117886

Cited by 18 publications

(10 citation statements)

References 23 publications

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“…At first, we measured the OGG1 protein and mRNA expression after high glucose (HG) exposure for 0, 6, 12 and 24 hours. Consistent with previously studies[15, 17], our results showed that HG significantly reduced OGG1 expression (Fig.1A-C). Similarly, STZ-induced diabetic mice showed OGG1 level was decreased in the endothelium of aorta compared to control mice (Fig.…”

Section: Resultssupporting

confidence: 93%

“…8-Oxoguanine DNA Glycosylase 1 (OGG1), a DNA glycosylase enzyme, was reported to involve in vascular oxidative stress and pathological progression of atherosclerosis[15, 33]. OGG1 expression was controlled by diverse mechanisms.…”

Section: Discussionmentioning

confidence: 99%

“…Total RNA was extracted with Trizol reagent, as described before[15]. Then we measured the concentration of RNA via NanoDrop 2000 (Thermo Scientific).…”

Section: Methodsmentioning

confidence: 99%

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Metformin prevented high glucose-induced endothelial reactive oxygen species via OGG1 in an AMPKα-Lin-28 dependent pathway

Tao

Fan

Sun

et al. 2020

Preprint

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Metformin improved vascular function in obese type 2 diabetic patients. 8-oxoguanine glycosylase (OGG1), a main DNA glycosylase, was involved in vascular complications in diverse diseases. However, whether metformin suppressed endothelial ROS via OGG1 pathway was unclear. Human umbilical vein endothelial cells (HUVECs) were exposed to HG (high glucose) or HG with metformin. OGG1 and AMPfα levels were measured after metformin treatment while HG-caused ROS was measured by DHE prober. Diabetic mice were induced by daily intraperitoneal injections of streptozotocin (STZ). Metformin reduced Endothelial ROS caused by HG via upregulating OGG1. Additionally, OGG1 protein expression was dependent on its mRNA stability, which was reversed by genetic inhibition of AMPKα and Lin-28. The role of OGG1 on ROS stimulated by HG was partially dependent on NFKB/NOX4 pathway in HUVECs. These results suggested that metformin contacted HG-induced endothelial ROS via AMPKα/Lin-28/OGG1 pathway.

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Section: Resultssupporting

confidence: 93%

Section: Discussionmentioning

confidence: 99%

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Metformin prevented high glucose-induced endothelial reactive oxygen species via OGG1 in an AMPKα-Lin-28 dependent pathway

Tao

Fan

Sun

et al. 2020

Preprint

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“…18 – 21 ). It was thought that the effect of high glucose on these cellular behaviors might derive from glycation-induced oxidative stress 3 , 37 . Both hydrogen production (HTON + VIS + AA) and glucose depletion (HTON + VIS + STT) can make partial contributions to the apoptotic attenuation and proliferative recovery of the investigated cells, causing a synergetic effect of photocatalytic therapy with HTON + VIS (combined therapy group) (Fig.…”

Section: Resultsmentioning

confidence: 99%

Photocatalytic glucose depletion and hydrogen generation for diabetic wound healing

Chen

Zhu

et al. 2022

Nat Commun

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High-glucose microenvironment in the diabetic foot ulcer (DFU) causes excessive glycation and induces chronic inflammation, leading to the difficulty of DFU healing. Hydrogen-rich water bath can promote the healing of DFU in clinic by virtue of the anti-inflammatory effect of hydrogen molecules, but the long-term daily soaking counts against the formation of a scab and cannot change the high-glucose microenvironment, limiting the outcome of DFU therapy. In this work, photocatalytic therapy of diabetic wound is proposed for sustainable hydrogen generation and local glucose depletion by utilizing glucose in the high-glucose microenvironment as a sacrificial agent. Hydrogen-incorporated titanium oxide nanorods are developed to realize efficient visible light (VIS)-responsive photocatalysis for glucose depletion and hydrogen generation, achieving a high efficacy of diabetic wound healing. Mechanistically, local glucose depletion and hydrogen generation jointly attenuate the apoptosis of skin cells and promote their proliferation and migration by inhibiting the synthesis of advanced glycation end products and the expression of their receptors, respectively. The proposed VIS-photocatalytic strategy provides a solution for facile, safe and efficient treatment of DFU.

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“…Our data are in good agreement and extend this study, and further demonstrate that Nox4, rather than Nox1 and Nox2 subtypes is abundantly expressed in the mouse glomeruli. Yet, as revealed by several in vitro and in vivo studies, the expression of all Nox subtypes and the ensuing ROS overproduction are induced in various cell types in the kidney (i.e., endothelial cells, mesangial cells, podocytes) in response to diabetic conditions by molecular mechanisms that broadly implicate the activation of pro-inflammatory signalling pathways [ 52 , 53 , 54 , 55 , 56 ]. Consistent with this evidence, it was recently demonstrated that ROS overproduction driven by both Nox1 and Nox2 contribute to oxidative stress and kidney injury in diabetic mice [ 18 ].…”

Section: Discussionmentioning

confidence: 99%

Activated Histone Acetyltransferase p300/CBP-Related Signalling Pathways Mediate Up-Regulation of NADPH Oxidase, Inflammation, and Fibrosis in Diabetic Kidney

et al. 2021

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Accumulating evidence implicates the histone acetylation-based epigenetic mechanisms in the pathoetiology of diabetes-associated micro-/macrovascular complications. Diabetic kidney disease (DKD) is a progressive chronic inflammatory microvascular disorder ultimately leading to glomerulosclerosis and kidney failure. We hypothesized that histone acetyltransferase p300/CBP may be involved in mediating diabetes-accelerated renal damage. In this study, we aimed at investigating the potential role of p300/CBP in the up-regulation of renal NADPH oxidase (Nox), reactive oxygen species (ROS) production, inflammation, and fibrosis in diabetic mice. Diabetic C57BL/6J mice were randomized to receive 10 mg/kg C646, a selective p300/CBP inhibitor, or its vehicle for 4 weeks. We found that in the kidney of C646-treated diabetic mice, the level of H3K27ac, an epigenetic mark of active gene expression, was significantly reduced. Pharmacological inhibition of p300/CBP significantly down-regulated the diabetes-induced enhanced expression of Nox subtypes, pro-inflammatory, and pro-fibrotic molecules in the kidney of mice, and the glomerular ROS overproduction. Our study provides evidence that the activation of p300/CBP enhances ROS production, potentially generated by up-regulated Nox, inflammation, and the production of extracellular matrix proteins in the diabetic kidney. The data suggest that p300/CBP-pharmacological inhibitors may be attractive tools to modulate diabetes-associated pathological processes to efficiently reduce the burden of DKD.

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High glucose induced endothelial cell reactive oxygen species via OGG1/PKC/NADPH oxidase pathway

Cited by 18 publications

References 23 publications

Metformin prevented high glucose-induced endothelial reactive oxygen species via OGG1 in an AMPKα-Lin-28 dependent pathway

Metformin prevented high glucose-induced endothelial reactive oxygen species via OGG1 in an AMPKα-Lin-28 dependent pathway

Photocatalytic glucose depletion and hydrogen generation for diabetic wound healing

Activated Histone Acetyltransferase p300/CBP-Related Signalling Pathways Mediate Up-Regulation of NADPH Oxidase, Inflammation, and Fibrosis in Diabetic Kidney

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