scholarly journals Advanced Glycation End Products Enhance Macrophages Polarization into M1 Phenotype through Activating RAGE/NF-κB Pathway

2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Xian Jin ◽  
Tongqing Yao ◽  
Zhong’e Zhou ◽  
Jian Zhu ◽  
Song Zhang ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Macrophage Polarization ◽  
M2 Macrophage ◽  
Advanced Glycation ◽  
Alternatively Activated Macrophages ◽  
M1 Macrophage ◽  
Glycation End Products ◽  
End Products ◽  
Patients With Diabetes ◽  
M1 Phenotype

Atherosclerotic lesions are accelerated in patients with diabetes. M1 (classically activated in contrast to M2 alternatively activated) macrophages play key roles in the progression of atherosclerosis. Since advanced glycation end products (AGEs) are major pathogenic factors and active inflammation inducers in diabetes mellitus, this study assessed the effects of AGEs on macrophage polarization. The present study showed that AGEs significantly promoted macrophages to express IL-6 and TNF-α. M1 macrophage markers such as iNOS and surface markers including CD11c and CD86 were significantly upregulated while M2 macrophage markers such as Arg1 and CD206 remained unchanged after AGEs stimulation. AGEs significantly increased RAGE expression in macrophages and activated NF-κB pathway, and the aforementioned effects were partly abolished by administration of anti-RAGE antibody or NF-κB inhibitor PDTC. In conclusion, our results suggest that AGEs enhance macrophage differentiation into proinflammatory M1 phenotype at least partly via RAGE/NF-κB pathway activation.

Abstract 268: Advanced Glycation End Products Effect on the Polarization of Macrophages Cardiac After Acute Myocardial Infarction in Wistar Rats

2016 ◽  
Vol 119 (suppl_1) ◽  
Author(s):  
Juliana O Rangel ◽  
Bianca Fracasso ◽  
Amanda Phaelante ◽  
Fernanda Curuja ◽  
Daniel Sturza ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Cardiac Remodeling ◽  
Wistar Rats ◽  
Macrophage Polarization ◽  
Tissue Homogenate ◽  
Advanced Glycation ◽  
M1 Macrophages ◽  
Glycation End Products ◽  
End Products

Macrophage phenotypes play an important role in post-MI cardiac remodeling. M1 macrophages have a proinflammatory phenotype and are found in the heart early after MI whereas M2 macrophages arise after and replace M1 macrophages in order to mediate the resolution of inflammation and angiogenesis. Advanced glycation end products (AGE) may modulate macrophage polarization but its functional role in the context of post-MI remains incompletely understood. Our goal is to assess whether AGE can polarize macrophages in post-MI and interfere in cardiac remodeling. We have collected experimental data from 68 male Wistar rats (2-3 month-old) divided in 4 groups: sham, MI + 0.9% NaCl (i.p.), MI + methylglyoxal (AGE inducer, 17 mg/kg/day; i.p.); and MI + aminoguanidine (anti-AGE agent, 0.5 g/L in drinking water). Subgroups were euthanized on days 2, 6, and 10 days post-MI. The echocardiographic analysis did not show differences in ejection fraction or akinetic/hypokinetic area among the MI groups. Cytokine levels were assessed by multiplex analysis in cardiac tissue homogenate. There was an increase of proinflammatory cytokine IL-6 on 10th day after surgery in MI group at the remote area, while IL-1β and IL-12 showed reduction compared with the sham group. Anti-inflammatory cytokine IL-10 did not show any difference among the groups. Until now, it is not possible to conclude whether AGE can induce macrophage polarization in vivo. More analyses are necessary to respond our objective.

Methylglyoxal and Advanced Glycation End Products in Patients with Diabetes – What We Know so Far and the Missing Links

2017 ◽  
Vol 127 (08) ◽  
pp. 497-504 ◽  
Author(s):  
Jan Benedikt Groener ◽  
Dimitrios Oikonomou ◽  
Ruan Cheko ◽  
Zoltan Kender ◽  
Johanna Zemva ◽  
...  
Keyword(s):  
Advanced Glycation End Products ◽  
Absolute Risk ◽  
Diabetes Type ◽  
Diabetes Type 1 ◽  
Advanced Glycation ◽  
Glycation End Products ◽  
End Products ◽  
Patients With Diabetes

AbstractHyperglycemia explains the development of late diabetic complications in patients with diabetes type 1 and type 2 only partially. Most therapeutic efforts relying on intensive glucose control failed to decrease the absolute risk for complications by more than 10%, especially in patients with diabetes type 2. Therefore, alternative pathophysiological pathways have to be examined, in order to develop more individualized treatment options for patients with diabetes in the future. One such pathway might be the metabolism of dicarbonyls, among them methylglyoxal and the accumulation of advanced glycation end products. Here we review currently available epidemiological data on dicarbonyls and AGEs in association with human diabetes type 1 and type 2.

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