Regulation of RAGE for Attenuating Progression of Diabetic Vascular Complications

Win, Myat; Yamamoto, Yasuhiko; Munesue, Seiichi; Saito, Hiroyoshi; Han, Dong; Motoyoshi, So; Kamal, Tarek; Ohara, Takuro; Watanabe, Takeshi; Yamamoto, Hiroshi

doi:10.1155/2012/894605

Cited by 53 publications

(46 citation statements)

References 91 publications

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“…To examine the effects of anti-AGE antibody treatment on RAGE and nephrin expression on primary glomerulus cells culture, we exposed cultured glomerulus primary cells with anti-AGE antibody and AGE. In normal condition, podocytes and glomerular endothelial cells, among other renal cell types express RAGE [12]. Interaction of AGE-RAGE induce the activation of inflammatory signalling [10].…”

Section: Discussionmentioning

confidence: 99%

“…Signalling pathways which activated by AGE-RAGE are ERK (extracellular signal-regulated kinase)1/2, p38 MAPK (mitogen-activated-protein-kinase)-JNK (c-Jun N-terminal kinases), JAK (Janus-kinase)-STAT (signal transducer and activator of transcription), and Rac-Cdc42 [12]. Activation of inflammatory signalling pathways increasing of reactive oxygen species (ROS) and leads positive feed-forward loop of NF-KB activation which is induces RAGE expression [12]. In this study, we hypothesized that anti-AGE antibody inhibits RAGE expression.…”

Section: Discussionmentioning

confidence: 99%

“…This result indicated that both of polyclonal and monoclonal anti-AGE antibody could inhibit RAGE expressions. The possibility of mechanisms that are involved in inhibition of RAGE expression is polyclonal and monoclonal anti-AGE antibody inhibit interaction of AGE-RAGE that cause inhibition of NF-KB activation and other signalling pathways and leads to inhibition of RAGE expression [12].…”

Section: Discussionmentioning

confidence: 99%

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Role of Antibody Anti-AGE in the Expression of Nephrin and RAGE on Primary Glomerulus Cell Exposed with AGE

Salam

Lyrawati

Samsu

2017

JTLS

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Nephrin is associated with the initial stage of the loss of the permeability barrier in diabetic nephropathy. Interaction AGE-RAGE increases angiotensin II on Renin Angiotensin-Aldosterone System (RAAS) and activation of protein kinase c (PKC) which induce alterations in nephrin mRNA expression. Alterations of nephrin expression induce transformation of slit membrane structure and the permeability changes at the glomerular filtration barrier. Anti-AGE vaccination once may cause the changes of nephrin and RAGE expression and can prevent progression of diabetic nephropathy. This study used primary glomerulus cell culture obtained from renal of Wistar rat aged 3 months, weighing 200-300 grams and assigned into negative control group that exposed to BSA 100 µg/mL, positive control group that exposed to AGE-BSA 100 µg/mL, treatment group 1 that exposed to polyclonal anti-AGE antibody 5 µg/mL and AGE-BSA 100 µg/mL and treatment group 2 that exposed to monoclonal anti-CML antibody 5 µg/mL and AGE-BSA 100 µg/mL. Paired t-test with a 0.05 level of confidence results showed that there were significantly different v in level of RAGE expression between experimental groups with control groups. Administration of polyclonal anti-AGE antibody decreased RAGE expression compared to negative control (p = 0.188) and positive control (p = 0.000). RAGE expression did not differ significantly in administration of monoclonal anti-CML antibody compared to negative control but significant with positive control. Administration of monoclonal anti-CML antibody inhibited increasing of nephrin expression compared to negative and positive control (p = 0.73; 0.125). In conclusion, this study suggested that administration of polyclonal anti-AGE or monoclonal anti-CML antibody could inhibit increasing of RAGE and nephrin expression in glomerulus primary culture that exposed to AGE which is expected to prevent the progression of diabetic nephropathy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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Role of Antibody Anti-AGE in the Expression of Nephrin and RAGE on Primary Glomerulus Cell Exposed with AGE

Salam

Lyrawati

Samsu

2017

JTLS

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“…These include antihypertensive drugs (calcium channel blockers, angiotensin-converting enzyme inhibitors, angiotensin II receptor blockers), antidiabetic drugs (thiazolidinedione) and cholesterol-lowering drugs (statins). These drugs contain soluble RAGE and may prevent various diabetic complications by preventing AGE from binding to RAGE (42)(43)(44).…”

Section: Drugs That Cause Receptor Blockagementioning

confidence: 99%

Dietary glycotoxins and infant formulas

Kutlu

2016

Turk Pediatri Ars

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Advanced glycation end products constitute a complex group of compounds derived from the nonenzymatic glycation of proteins, lipids, and nucleic acids formed endogenously, but also from exogenous supplies such as tobacco smoking (glycotoxins). Accumulating evidence underlies the beneficial effect of the dietary restriction of glycotoxins in animal studies and also in patients with diabetic complications and metabolic diseases. Composition of infant formulas and their processing methods render an extraordinary favorable milieu for the formation of glycotoxins, and the content of glycotoxins in infant formula exceeds that of breast milk by hundred folds. Data from a limited number of short-term small studies in healthy infants do not provide direct evidence of acute negative health effects of glycotoxins in early infancy. However, the effects in sensitive groups on the state of future health in adulthood remain unclear. (Turk Pediatri Ars 2016; 51: 179-85)

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“…Kollagenvernetzung durch AGEs, Elastinschwund und Mediakalzinose bedingen dabei Wandverhärtung und verminderte Dehnbarkeit der Arterien; sie fördern so Hypertonie und erhöhte Atheroskleroseprogredienz [56,148]. Auch glykierte LDLs und HDLs könnten eine wichtige Rolle bei der Atherogenese spielen [158].…”

Section: Schlussfolgerungenunclassified

Aktuelles zur diabetischen Makroangiopathie

Kunz¹

2012

Pathologe

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Current findings from the literature on the multifactorial genesis of macroangiopathy of diabetes mellitus (DM) were compiled using the PubMed database. The primary aim was to find an explanation for the morphological, immunohistochemical and molecular characteristics of this form of atherosclerosis. The roles of advanced glycation end products (AGE), defective signal transduction and imbalance of matrix metalloproteinases in the increased progression of atherosclerosis in coronary and cerebral arteries as well as peripheral vascular disease are discussed. The restricted formation of collateral arteries (arteriogenesis) in diabetic patients with postischemic lesions is also a focus of attention. The increased level of prothrombotic factors and the role of diabetic neuropathy in DM are also taken into account. Therapeutic influences of AGE-RAGE (receptor of AGE) interactions on the vascular wall and the effects of endothelial progenitor cells in the repair of diabetic vascular lesions are additionally highlighted.

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Regulation of RAGE for Attenuating Progression of Diabetic Vascular Complications

Cited by 53 publications

References 91 publications

Role of Antibody Anti-AGE in the Expression of Nephrin and RAGE on Primary Glomerulus Cell Exposed with AGE

Role of Antibody Anti-AGE in the Expression of Nephrin and RAGE on Primary Glomerulus Cell Exposed with AGE

Dietary glycotoxins and infant formulas

Aktuelles zur diabetischen Makroangiopathie

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