Expression modification of uncoupling proteins and MnSOD in retinal endothelial cells and pericytes induced by high glucose: The role of reactive oxygen species in diabetic retinopathy

Cui, Yan; Xu, Xun; Bi, Hongsheng; Zhu, Qi; Wu, Jianfeng; Xia, Xin; Ren, Qian; Ho, Pak‐Chung

doi:10.1016/j.exer.2006.03.024

Cited by 141 publications

(115 citation statements)

References 21 publications

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“…30 Moreover, the protective role of UCP2 in the pathogenesis of diabetic retinopathy has been identified. 31 In the present study, we demonstrated that UCP2 was induced in the tubular epithelial cells under the condition of hyperglycemia as a compensative reaction for ROS overproduction. To test the hypothesis that UCP2 functions to limit ROS production, we used genipin, a UCP2 inhibitor, to inhibit uncoupling protein expression.…”

Section: Discussionmentioning

confidence: 72%

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

Chen

Tang

et al. 2014

Renal Failure

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Renal tubular epithelial cell injury is a major pathological event that contributes to the development of diabetic kidney disease (DKD). Uncoupling protein-2 (UCP2), a mitochondrial membrane protein, has been reported to participate in the regulation of reactive oxygen species (ROS) generation, which contributes to tubular cell apoptosis induced by hyperglycemia. In this study, we found that genipin, a UCP2 inhibitor, dramatically boosted oxidative stress, attenuated antioxidative capacity, and exacerbated cell apoptosis accompanied with caspase-3 activation in rat renal proximal tubular cells (NRK-52E) incubated with high glucose. The present study results suggest that manipulation of UCP2 could be important in the prevention of oxidative stress damage in renal tubular epithelial cells induced by hyperglycemia in vitro.

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Section: Discussionmentioning

confidence: 72%

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

Chen

Tang

et al. 2014

Renal Failure

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“…Thereafter, the cells were characterized for their homogeneity using an immunoreactivity test with anti-factor VIII antibody for BRECs. 16,17 Only cells of passages 5-10 were used for this study. Cells were seeded into 60 mm plates (5 Â 10 4 cells/ml, 4 ml) and were incubated with 5 or 30 mM glucose for 3 days.…”

Section: Cell Culture and Study Designmentioning

confidence: 99%

“…16 The cells were subsequently cultured with Dulbecco's modified Eagle's medium supplemented with 10% FBS (GIBCO), 100 mg/l heparin (Sigma), 10 mmol/l HEPES (GIBCO), and 15 mg/l ECGS (Sigma). The culture plate (corning) was coated with Gelatin (Sigma) beforehand.…”

Section: Cell Culture and Study Designmentioning

confidence: 99%

High glucose attenuates insulin-induced VEGF expression in bovine retinal microvascular endothelial cells

Xia

Jiang

et al. 2009

Eye

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“…At high membrane potential, a small increase in membrane potential gives rise to production of significant amounts of ROS [210,211]. Nutrient excess and metabolic inflexibility are a major cause of increased mitochondrial ROS production and oxidative stress [156,203,212]. These perturbations of blunted fuel switching and distorted nutrient sensing have been described in a variety of clinical settings, including obesity and diabetes, as well as in various organs and cell types, like adipose tissues, macrophages and monocytes [203].…”

Section: Ir Nutrient Excess Mitochondrial Inflexibility and Rosmentioning

confidence: 99%

“…Aging is associated with a whole series of metabolic alterations related to the development of cancer, like increased ROS production and damage to mitochondria with mitochondrial dysfunction (including stem cells) [155,212,216], insulin resistance and hyperinsulinemia including activation of the IGF system [39], glucose intolerance [38], increased SNS activity [217], and a progressive increase in total body fat in the general population with advancing age [218].…”

Section: Cancer Risk Factors and Related Metabolic Alterationsmentioning

confidence: 99%

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

Köpp¹

2017

J Carcinog Mutagen

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In all western societies, mortality rates from cancer are high and even increasing. In striking contrast, cancer rates are very rare and even non-existent in primitive cultures, like hunter-gatherer (HG) populations. HGs are free of disease as long as they adhere to their traditional low-insulinemic "Paleolithic" nutrition. With acculturation and transition to current high-carbohydrate/high-insulinemic "Western" diets (HCHIDs), cancer develops in high rates. This paper follows the question of how significant nutritional changes, brought about by the Agricultural revolution, may cause development of cancer. The evidence presented shows that the switch from a Paleolithic to a Western nutrition has brought about significant metabolic perturbations, like an abnormally increased activation of the insulinlike growth factor system, the sympathetic nervous system and the renin-angiotensin-system, an increased expression of HIF-1α and other more, all of which are deeply involved in cancer development through promotion of proliferation, angiogenesis, inflammation, macrophage infiltration, metastasis and inhibition of apoptosis.In addition, HCHIDs generate oxidative stress which may cause mitochondrial damage and genomic instability, and may interfere with normal stem cell development. Faulty redox signaling is suggested to play a significant role in cancer development: hydrogen peroxide, generated at low concentrations, represents an important chemical mediator in the regulation of various cellular signal transduction processes, including stem cell development. Oxidative stress may be sensed by cells as redox signaling. Faulty "redox signaling" is proposed to affect normal stem cell development by sustained activation of uncoupling protein 2, leading to inhibition of differentiation ("maturation arrest"), sustained uncontrolled proliferation, and glycolysis with high expression of hexokinase II, typical features of cancer. In summary, an abnormal diet-related activation of various metabolic systems, together with faulty redox signaling, is suggested to play a pivotal role in cancer development.

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Expression modification of uncoupling proteins and MnSOD in retinal endothelial cells and pericytes induced by high glucose: The role of reactive oxygen species in diabetic retinopathy

Cited by 141 publications

References 21 publications

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

Downregulation of uncoupling protein-2 by genipin exacerbates diabetes-induced kidney proximal tubular cells apoptosis

High glucose attenuates insulin-induced VEGF expression in bovine retinal microvascular endothelial cells

Significant Dietary Changes during Human Evolution and the Development of Cancer: From Cells in Trouble to Cells Causing Trouble

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