Glycated albumin induces lipid infiltration in mice aorta independently of DM and RAS local modulation by inducing lipid peroxidation and inflammation

Glycated albumin induces lipid infiltration in mice aorta independently of DM and RAS local modulation by inducing lipid peroxidation and inflammation

Abstract Aims Advanced glycated albumin (AGE-albumin) adversely impairs macrophage lipid homeostasis in vitro, which may be prevented by angiotensin receptor blockers. In vivo studies are inconclusive whether AGE-albumin itself plays important role in early-stage atherogenesis. We aimed at investiga...

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Published in:Journal of diabetes and its complications Vol. 30; no. 8; pp. 1614 - 1621
Main Authors: Gomes, D.J, Velosa, A.P, Okuda, L.S, Fusco, F.B, Silva, K.S, Pinto, P.R, Nakandakare, E.R, Correa-Giannella, M.L, Woods, T, Brimble, M.A, Pickford, R, Rye, K.A, Teodoro, W.R, Catanozi, S, Passarelli, M
Format: Journal Article
Language:English
Published: United States Elsevier Inc 01-11-2016
Elsevier Limited
Subjects:
Advanced glycation
Age
Animals
Aorta - pathology
Atherosclerosis
Atherosclerosis - physiopathology
Cholesterol
Coronary vessels
Diabetes
Diabetes Mellitus, Experimental - physiopathology
Drinking water
Dyslipidemias - physiopathology
Endocrinology & Metabolism
Glycated albumin
Inflammation
Inflammation - pathology
Laboratory animals
Lipid Peroxidation
Lipids
Losartan
Male
Mass spectrometry
Mice
Mice, Inbred C57BL
Mice, Knockout
Oxidative stress
Proteins
Renin-Angiotensin System
Scientific imaging
Serum Albumin - administration & dosage
Studies
Triglycerides
atherosclerosis
advanced glycation
glycated albumin
losartan
inflammation
oxidative stress
Glycated albumin
Oxidative stress
Inflammation
Advanced glycation
Losartan
Atherosclerosis
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Summary:Abstract Aims Advanced glycated albumin (AGE-albumin) adversely impairs macrophage lipid homeostasis in vitro, which may be prevented by angiotensin receptor blockers. In vivo studies are inconclusive whether AGE-albumin itself plays important role in early-stage atherogenesis. We aimed at investigating how AGE-albumin by itself drives atherosclerosis development in dyslipidemic non-diabetic mice and if its effects are due to the activation of renin-angiotensin system in the arterial wall and the expression of genes and proteins involved in lipid flux. Methods and Results Murine albumin glycation was induced by incubation with 10 mM glycolaldehyde and C-albumin with PBS alone. Twelve-week-old-male apoE knockout mice were submitted to a daily IP injection of control (C) or AGE-albumin (2 mg) during 30 days with or without losartan (LOS - 100 mg/L; C + LOS and AGE + LOS). Aortic arch was removed and gene expression determined by RT-PCR; protein content by immunofluorescence. Plasma lipid and glucose levels were similar among groups. Systolic blood pressure was similarly reduced in both groups treated with LOS. In comparison to C-albumin, aortic lipid infiltration was 5.3 times increased by AGE-albumin, which was avoided by LOS. LOS prevented the enhancement induced by AGE-albumin in Ager, Tnf and Cybb mRNA levels but did not reduce Olr1. Nfkb and Agt mRNA levels were unchanged by AGE-albumin. LOS similarly reduced Agtr1a mRNA level in both C and AGE-albumin groups. In AGE-albumin-treated mice, immunofluorescence for carboxymethyl-lysine, 4-hydroxynonenal and RAGE was respectively, 4.8, 2.6 and 1.7 times enhanced in comparison to C-albumin. These increases were all avoided by LOS. Conclusions AGE-albumin evokes a pre-stage of atherogenesis in dyslipidemic mice independently of the presence of diabetes mellitus or modulation in the RAS in parts, by the induction of lipid peroxidation and inflammation.
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ISSN:1056-8727
1873-460X
DOI:10.1016/j.jdiacomp.2016.07.001