Role of moesin, Src, and ROS in advanced glycation end product‐induced vascular endothelial dysfunction

Zhang, Weijin; Li, Peixin; Guo, Xiaohua; Huang, Qiaobing

doi:10.1111/micc.12358

Cited by 35 publications

(35 citation statements)

References 44 publications

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“…It has been widely reported that high levels of ROS is a key factor in vascular injury [37] and dysfunction [38]. The present study demonstrated that Ang II-mediated endogenous oxidative stress triggered vascular endothelial cell apoptosis, which may be the molecular mechanism associated with Ang II-induced vascular injury.…”

Section: Discussionsupporting

confidence: 59%

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

et al. 2017

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Introduction: This study aimed to investigate whether epigallocatechin-3-gallate (EGCG) shows antioxidant activity against angiotensin II (Ang II)-induced human umbilical vein endothelial cell (HUVEC) apoptosis. Materials and Methods: The viability of HUVECs was revealed by MTT and LDH assay. The cell apoptosis was detected by FITC-PI assay. A fluorescent probe assay was used to measure the reactive oxygen species (ROS) generation in HUVECs. Mitochondrial permeability transition pore (MPTP) opening, mitochondrial membrane potential, and caspase-3, -4, -8, -9 activities were also measured. Results: We found that Ang II treatment increased the generation of ROS, enhanced MPTP opening and cytochrome c release, activated caspase-3/9, and consequently induced HUVEC apoptosis. EGCG treatment-suppressed Ang II induces the oxidative stress of HUVECs and mitochondria-related cell apoptosis. We also showed that the antioxidant activity pathway, including cytochrome c release, MPTP opening, and caspase-3/9 activation, is a key endogenous defensive system in HUVECs, provoking Ang II exposure. Our study revealed that increased expression of Nrf2 by EGCG could partially repress Ang II-induced injury effects. Conclusions: All of our findings indicated that EGCG treatment provides a protective effect for Ang II-induced HUVEC apoptosis by decreasing oxidative stress and ameliorating mitochondrial injury.

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Section: Discussionsupporting

confidence: 59%

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

et al. 2017

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“…In contrast, insufficient silicon intake is associated with a high risk of cardiovascular events and increases the case fatality rate [84]. Selenium often acts as a redox scavenger in the human body [27], an action which is essential to the restoration of impaired islets and vascular tissues in diabetes [85,86]. The liver is one of the organs with the highest selenium concentration [87].…”

Section: Elementsmentioning

confidence: 99%

Trace Elements, PPARs, and Metabolic Syndrome

Shi

Zou

Shen

et al. 2020

IJMS

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Metabolic syndrome (MetS) is a constellation of metabolic derangements, including central obesity, insulin resistance, hypertension, glucose intolerance, and dyslipidemia. The pathogenesis of MetS has been intensively studied, and now many factors are recognized to contribute to the development of MetS. Among these, trace elements influence the structure of proteins, enzymes, and complex carbohydrates, and thus an imbalance in trace elements is an independent risk factor for MetS. The molecular link between trace elements and metabolic homeostasis has been established, and peroxisome proliferator-activated receptors (PPARs) have appeared as key regulators bridging these two elements. This is because on one hand, PPARs are actively involved in various metabolic processes, such as abdominal adiposity and insulin sensitivity, and on the other hand, PPARs sensitively respond to changes in trace elements. For example, an iron overload attenuates hepatic mRNA expression of Ppar-α; zinc supplementation is considered to recover the DNA-binding activity of PPAR-α, which is impaired in steatotic mouse liver; selenium administration downregulates mRNA expression of Ppar-γ, thereby improving lipid metabolism and oxidative status in the liver of high-fat diet (HFD)-fed mice. More importantly, PPARs' expression and activity are under the control of the circadian clock and show a robust 24 h rhythmicity, which might be the reasons for the side effects and the clinical limitations of trace elements targeting PPARs. Taken together, understanding the casual relationships among trace elements, PPARs' actions, and the pathogenesis of MetS is of great importance. Further studies are required to explore the chronopharmacological effects of trace elements on the diurnal oscillation of PPARs and the consequent development of MetS.

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“…Aberrant crosslinks between AGEs and key molecules of extracellular matrix result in a decrease in the elasticity and an increase the stiffness of vessels, consequently increase the thickness and rigidity of the vessel wall [14,15]. In addition, binding of AGEs to different cellular receptors can trigger multiple cell signaling pathways.…”

Section: Ages and Age-rage Interactionmentioning

confidence: 99%

“…However, in diabetes, certain inflammatory stimulates target ECs, resulting in hyperpermeability [15]. Therefore, the ensuing impairment of BRB further induces macular edema and vascular hemorrhage, compromising retina integrity [33].…”

Section: Endothelial Dysfunctionmentioning

confidence: 99%

Involvement of Advanced Glycation End Products in the Pathogenesis of Diabetic Retinopathy

Chen

et al. 2018

Cell Physiol Biochem

157

106

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Diabetic retinopathy (DR) is a common and devastating microvascular complication of diabetes and a major cause of acquired blindness in young adults. Advanced glycation end products (AGEs) accumulated under hyperglycemic conditions are thought to play an important role in the pathogenesis of DR. AGEs can exert their deleterious effects by acting directly to induce aberrant crosslinking of extracellular matrix proteins, to increase vascular stiffness, altering vascular structure and function. Moreover, AGEs binding to the receptor for AGEs (RAGE) evokes intensive intracellular signaling cascades that leading to endothelial dysfunction, elaboration of key proinflammatory cytokines and proangiogenic factors, mediating pericyte apoptosis, vascular inflammation and angiogenesis, as well as breakdown of the inner blood-retinal barrier (BRB), the end result of all these events is damage to the neural and vascular components of the retina. Elucidation of AGE-induced mechanisms will help in the understanding of the complex cellular and molecular pathogenesis associated with DR. Novel anti-AGEs agents or AGE crosslink “breakers” are being investigated, it is hoped that in next few years, some of these promising therapies will be successfully applied in clinical context, aiming to reduce the major economical and medical burden caused by DR.

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Role of moesin, Src, and ROS in advanced glycation end product‐induced vascular endothelial dysfunction

Cited by 35 publications

References 44 publications

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

Epigallocatechin-3-Gallate Ameliorates Angiotensin II-Induced Oxidative Stress and Apoptosis in Human Umbilical Vein Endothelial Cells through the Activation of Nrf2/Caspase-3 Signaling

Trace Elements, PPARs, and Metabolic Syndrome

Involvement of Advanced Glycation End Products in the Pathogenesis of Diabetic Retinopathy

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