Advanced glycation end-products disrupt brain microvascular endothelial cell barrier: The role of mitochondria and oxidative stress

Dobi, Anthony; Rosanaly, Sarah; Devin, Anne; Baret, Pascal; Meilhac, Olivier; Harry, G. Jean; d’Hellencourt, Christian Lefebvre; Rondeau, Philippe

doi:10.1016/j.mvr.2020.104098

Cited by 28 publications

(18 citation statements)

References 88 publications

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“…Recent research findings strongly suggest that AGEs are the main contributors to brain microvascular damage and disruption of the blood–brain barrier (BBB) [ 260 ]. Interactions between the BBB, cerebral blood vessels, neurons, astrocytes, microglia and pericytes form a dynamic functional neurovascular unit.…”

Section: Role Of Modified Albumin In Pathogenesis Of Diseasesmentioning

confidence: 99%

Serum Albumin in Health and Disease: Esterase, Antioxidant, Transporting and Signaling Properties

Belinskaia

Voronina

Шмурак

et al. 2021

IJMS

142

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Being one of the main proteins in the human body and many animal species, albumin plays a decisive role in the transport of various ions—electrically neutral and charged molecules—and in maintaining the colloidal osmotic pressure of the blood. Albumin is able to bind to almost all known drugs, as well as many nutraceuticals and toxic substances, largely determining their pharmaco- and toxicokinetics. Albumin of humans and respective representatives in cattle and rodents have their own structural features that determine species differences in functional properties. However, albumin is not only passive, but also an active participant of pharmacokinetic and toxicokinetic processes, possessing a number of enzymatic activities. Numerous experiments have shown esterase or pseudoesterase activity of albumin towards a number of endogeneous and exogeneous esters. Due to the free thiol group of Cys34, albumin can serve as a trap for reactive oxygen and nitrogen species, thus participating in redox processes. Glycated albumin makes a significant contribution to the pathogenesis of diabetes and other diseases. The interaction of albumin with blood cells, blood vessels and tissue cells outside the vascular bed is of great importance. Interactions with endothelial glycocalyx and vascular endothelial cells largely determine the integrative role of albumin. This review considers the esterase, antioxidant, transporting and signaling properties of albumin, as well as its structural and functional modifications and their significance in the pathogenesis of certain diseases.

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Section: Role Of Modified Albumin In Pathogenesis Of Diseasesmentioning

confidence: 99%

Serum Albumin in Health and Disease: Esterase, Antioxidant, Transporting and Signaling Properties

Belinskaia

Voronina

Шмурак

et al. 2021

IJMS

142

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“…Exercise training can also improve brain function in insulin resistance states. In diabetes, advanced glycation end-products (AGEs) are considered to contribute to the development of alterations in cerebral capillaries, leading to a disruption of the blood-brain barrier [67]. Briefly, AGEs (macromolecules formed by a process known as glycation that occurs when glucose reacts with proteins, lipids, and nucleic acids after chronic exposure to hyperglycemia) are widely distributed in the body and their accumulation can affect the vascular basement membrane and extracellular matrices [68].…”

Section: The Long-term Effects Of Regular Exercise On Glycemic Control and Overall Health In Insulin Resistance Statesmentioning

confidence: 99%

“…Briefly, AGEs (macromolecules formed by a process known as glycation that occurs when glucose reacts with proteins, lipids, and nucleic acids after chronic exposure to hyperglycemia) are widely distributed in the body and their accumulation can affect the vascular basement membrane and extracellular matrices [68]. The accumulation of AGEs in the brain upregulates inflammatory cytokines and adhesion molecules, leading to chronic inflammation, amplified oxidative stress, and cerebral microvascular endothelial cell damage [67,69]. While AGEs increase during normal aging [70], their formation accelerates in diabetes, and this has been considered one of the possible links of diabetes and the development of cognitive impairments [69].…”

Section: The Long-term Effects Of Regular Exercise On Glycemic Control and Overall Health In Insulin Resistance Statesmentioning

confidence: 99%

Exercise as a Therapeutic Intervention in Gestational Diabetes Mellitus

et al. 2021

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Gestational Diabetes Mellitus (GDM) is defined as any degree of glucose intolerance with onset or first recognition during pregnancy. Regular exercise is important for a healthy pregnancy and can lower the risk of developing GDM. For women with GDM, exercise is safe and can affect the pregnancy outcomes beneficially. A single exercise bout increases skeletal muscle glucose uptake, minimizing hyperglycemia. Regular exercise training promotes mitochondrial biogenesis, improves oxidative capacity, enhances insulin sensitivity and vascular function, and reduces systemic inflammation. Exercise may also aid in lowering the insulin dose in insulin-treated pregnant women. Despite these benefits, women with GDM are usually inactive or have poor participation in exercise training. Attractive individualized exercise programs that will increase adherence and result in optimal maternal and offspring benefits are needed. However, as women with GDM have a unique physiology, more attention is required during exercise prescription. This review (i) summarizes the cardiovascular and metabolic adaptations due to pregnancy and outlines the mechanisms through which exercise can improve glycemic control and overall health in insulin resistance states, (ii) presents the pathophysiological alterations induced by GDM that affect exercise responses, and (iii) highlights cardinal points of an exercise program for women with GDM.

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“…In the present study, we used 661w cells treated with AGEs as a model to explore the regulation of AMPK on mitochondria and autophagy in the context of diabetes. AGEs can destroy the biological function of mitochondria [19] and inhibit normal autophagy in cells [20], which provides an important platform for researchers to study the molecular mechanisms and drug interventions associated with mitochondrial and autophagy-related central nervous system diseases. Some studies reported that AMPK showed protective effects on different cell lines, such as podocytes [21], hippocampal neurons [22], retinal pigment epithelium ARPE-19 cells [23], and Müller cells [24].…”

Section: Discussionmentioning

confidence: 99%

Stimulation of AMPK Prevents Diabetes‐Induced Photoreceptor Cell Degeneration

Song

Bao

Zhang

et al. 2021

Oxidative Medicine and Cellular Longevity

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Diabetic retinopathy (DR) is a kind of severe retinal neurodegeneration. The advanced glycation end products (AGEs) affect autophagy, and mitochondrial function is involved in DR. Adenosine-activated protein kinase (AMPK) is an important metabolic sensor that can regulate energy homeostasis in cells. However, the effect of AMPK in DR is still not fully understood. In this study, we investigated the effect of AMPK on diabetes-induced photoreceptor cell degeneration. In vivo, a diabetic mouse model was established by streptozotocin (STZ) injection. Haematoxylin-eosin (HE) staining was used to observe retinal morphology and measure the thicknesses of different layers in the retina. Electroretinogram (ERG) was used to evaluate retinal function. In vitro, 661w cells were treated with AGEs with/without an AMPK agonist (metformin) or AMPK inhibitor (compound C). Flow cytometry and CCK-8 assays were used to analyse apoptosis. Mitochondrial membrane potential was analysed by JC-1. Western blotting and qRT-PCR were used to examine the expression of related proteins and genes, respectively. The wave amplitude and the thickness of the outer nuclear layer were decreased in diabetic mice. The expression of rhodopsin and opsin was also decreased in diabetic mice. In vitro, the percentage of apoptotic cells was increased, the expression of the apoptosis-related protein Bax was increased, and Bcl-2 was decreased after AGE treatment in 661w cells. The expression of the autophagy-related protein LC3 was decreased, and p62 was increased. The mitochondrial-related gene expression and membrane potential were decreased, and mitochondrial morphology was abnormal, as observed by TEM. However, AMPK stimulation ameliorated this effect. These results indicate that AMPK stimulation can delay diabetes-induced photoreceptor degeneration by regulating autophagy and mitochondrial function.

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Advanced glycation end-products disrupt brain microvascular endothelial cell barrier: The role of mitochondria and oxidative stress

Cited by 28 publications

References 88 publications

Serum Albumin in Health and Disease: Esterase, Antioxidant, Transporting and Signaling Properties

Serum Albumin in Health and Disease: Esterase, Antioxidant, Transporting and Signaling Properties

Exercise as a Therapeutic Intervention in Gestational Diabetes Mellitus

Stimulation of AMPK Prevents Diabetes‐Induced Photoreceptor Cell Degeneration

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