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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{"_id":"63Ek9pSuD5AAdTbxu","bibbaseid":"grossin-auger-niquetleridon-durieux-montaigne-schmidt-susen-jacolot-etal-dietarycmlenrichedproteininducesfunctionalarterialaginginaragedependentmannerinmice-2015","author_short":["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."],"bibdata":{"bibtype":"article","type":"article","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\\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.","language":"ENG","journal":"Molecular Nutrition & Food Research","author":[{"propositions":[],"lastnames":["Grossin"],"firstnames":["Nicolas"],"suffixes":[]},{"propositions":[],"lastnames":["Auger"],"firstnames":["Florent"],"suffixes":[]},{"propositions":[],"lastnames":["Niquet-Leridon"],"firstnames":["Céline"],"suffixes":[]},{"propositions":[],"lastnames":["Durieux"],"firstnames":["Nicolas"],"suffixes":[]},{"propositions":[],"lastnames":["Montaigne"],"firstnames":["David"],"suffixes":[]},{"propositions":[],"lastnames":["Schmidt"],"firstnames":["Ann","Marie"],"suffixes":[]},{"propositions":[],"lastnames":["Susen"],"firstnames":["Sophie"],"suffixes":[]},{"propositions":[],"lastnames":["Jacolot"],"firstnames":["Philippe"],"suffixes":[]},{"propositions":[],"lastnames":["Beuscart"],"firstnames":["Jean-Baptiste"],"suffixes":[]},{"propositions":[],"lastnames":["Tessier"],"firstnames":["Frédéric","J."],"suffixes":[]},{"propositions":[],"lastnames":["Boulanger"],"firstnames":["Eric"],"suffixes":[]}],"month":"February","year":"2015","pmid":"25655894","bibtex":"@article{grossin_dietary_2015,\n\ttitle = {Dietary {CML}-enriched protein induces functional arterial aging in a {RAGE}-dependent manner in mice},\n\tissn = {1613-4133},\n\tdoi = {10.1002/mnfr.201400643},\n\tabstract = {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.\nMETHODS 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.\nCONCLUSION:: 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.},\n\tlanguage = {ENG},\n\tjournal = {Molecular Nutrition \\& Food Research},\n\tauthor = {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},\n\tmonth = feb,\n\tyear = {2015},\n\tpmid = {25655894},\n}\n\n","author_short":["Grossin, N.","Auger, F.","Niquet-Leridon, C.","Durieux, N.","Montaigne, D.","Schmidt, A. M.","Susen, S.","Jacolot, P.","Beuscart, J.","Tessier, F. 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