Dietary CML-enriched protein induces functional arterial aging in a RAGE-dependent manner in mice. Grossin, N., Auger, F., Niquet-Leridon, C., Durieux, N., Montaigne, D., Schmidt, A. M., Susen, S., Jacolot, P., Beuscart, J., Tessier, F. J., & Boulanger, E. Molecular Nutrition & Food Research, February, 2015.
doi  abstract   bibtex   
SCOPE:: Advanced glycation end-products (AGEs) are endogenously produced and are present in food. N(ε) -carboxymethyllysine (CML) is an endothelial activator via the receptor for AGEs (RAGE) and is a major dietary AGE. This work investigated the effects of a CML-enriched diet and RAGE involvement in aortic aging in mice. METHODS AND RESULTS:: After 9 months of a control diet or CML-enriched diets (50, 100 or 200μgCML /g of food), endothelium-dependent relaxation (EDR), RAGE, vascular cell adhesion molecule-1 (VCAM-1) and sirtuin-1 (SIRT1) expression, pulse wave velocity (PWV) and elastin disruption were measured in aortas of wild-type or RAGE(-/-) male C57BL/6 mice. Compared to the control diet, EDR was reduced in the wild-type mice fed the CML-enriched diet (200μgCML /g) (66.8±12.26 vs 94.3±2.6%, p\textless0.01). RAGE and VCAM-1 (p\textless0.05) expression were increased in the aortic wall. RAGE(-/-) mice were protected against CML-enriched diet-induced endothelial dysfunction. Compared to control diet, the CML-enriched diet (200μgCML /g) increased the aortic PWV (86.6±41.1 vs 251.4±41.1cm/s, p\textless0.05) in wild-type animals. Elastin disruption was found to a greater extent in the CML-fed mice (p\textless0.05). RAGE(-/-) mice fed the CML-enriched diet were protected from aortic stiffening. CONCLUSION:: Chronic CML ingestion induced endothelial dysfunction and arterial stiffness and aging in a RAGE dependent manner. This article is protected by copyright. All rights reserved.
@article{grossin_dietary_2015,
	title = {Dietary {CML}-enriched protein induces functional arterial aging in a {RAGE}-dependent manner in mice},
	issn = {1613-4133},
	doi = {10.1002/mnfr.201400643},
	abstract = {SCOPE:: Advanced glycation end-products (AGEs) are endogenously produced and are present in food. N(ε) -carboxymethyllysine (CML) is an endothelial activator via the receptor for AGEs (RAGE) and is a major dietary AGE. This work investigated the effects of a CML-enriched diet and RAGE involvement in aortic aging in mice.
METHODS AND RESULTS:: After 9 months of a control diet or CML-enriched diets (50, 100 or 200μgCML /g of food), endothelium-dependent relaxation (EDR), RAGE, vascular cell adhesion molecule-1 (VCAM-1) and sirtuin-1 (SIRT1) expression, pulse wave velocity (PWV) and elastin disruption were measured in aortas of wild-type or RAGE(-/-) male C57BL/6 mice. Compared to the control diet, EDR was reduced in the wild-type mice fed the CML-enriched diet (200μgCML /g) (66.8±12.26 vs 94.3±2.6\%, p{\textless}0.01). RAGE and VCAM-1 (p{\textless}0.05) expression were increased in the aortic wall. RAGE(-/-) mice were protected against CML-enriched diet-induced endothelial dysfunction. Compared to control diet, the CML-enriched diet (200μgCML /g) increased the aortic PWV (86.6±41.1 vs 251.4±41.1cm/s, p{\textless}0.05) in wild-type animals. Elastin disruption was found to a greater extent in the CML-fed mice (p{\textless}0.05). RAGE(-/-) mice fed the CML-enriched diet were protected from aortic stiffening.
CONCLUSION:: Chronic CML ingestion induced endothelial dysfunction and arterial stiffness and aging in a RAGE dependent manner. This article is protected by copyright. All rights reserved.},
	language = {ENG},
	journal = {Molecular Nutrition \& Food Research},
	author = {Grossin, Nicolas and Auger, Florent and Niquet-Leridon, Céline and Durieux, Nicolas and Montaigne, David and Schmidt, Ann Marie and Susen, Sophie and Jacolot, Philippe and Beuscart, Jean-Baptiste and Tessier, Frédéric J. and Boulanger, Eric},
	month = feb,
	year = {2015},
	pmid = {25655894},
}

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