Standard

Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice. / Hanssen, Nordin M. J.; Tikellis, Chris; Pickering, Raelene J. et al.

In: Biomedicine and Pharmacotherapy, Vol. 158, 114211, 01.02.2023.

Research output: Contribution to journal › Article › Academic › peer-review

Harvard

Hanssen, NMJ, Tikellis, C, Pickering, RJ, Dragoljevic, D, Lee, MKS, Block, T, Scheijen, JLJM, Wouters, K, Miyata, T, Cooper, ME, Murphy, AJ, Thomas, MC & Schalkwijk, CG 2023, 'Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice', Biomedicine and Pharmacotherapy, vol. 158, 114211. https://doi.org/10.1016/j.biopha.2022.114211

APA

Hanssen, N. M. J., Tikellis, C., Pickering, R. J., Dragoljevic, D., Lee, M. K. S., Block, T., Scheijen, J. L. JM., Wouters, K., Miyata, T., Cooper, M. E., Murphy, A. J., Thomas, M. C., & Schalkwijk, C. G. (2023). Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice. Biomedicine and Pharmacotherapy, 158, [114211]. https://doi.org/10.1016/j.biopha.2022.114211

Vancouver

Hanssen NMJ, Tikellis C, Pickering RJ, Dragoljevic D, Lee MKS, Block T et al. Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice. Biomedicine and Pharmacotherapy. 2023 Feb 1;158:114211. doi: 10.1016/j.biopha.2022.114211

Author

Hanssen, Nordin M. J. ; Tikellis, Chris ; Pickering, Raelene J. et al. / Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice. In: Biomedicine and Pharmacotherapy. 2023 ; Vol. 158.

BibTeX

@article{349c407cbb6c4364aeaa7d60a055fe8e,
title = "Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice",
abstract = "Methylglyoxal (MGO) is a reactive glucose metabolite linked to diabetic cardiovascular disease (CVD). MGO levels surge during intermittent hyperglycemia. We hypothesize that these MGO spikes contribute to atherosclerosis, and that pyridoxamine as a MGO quencher prevents this injury. To study this, we intravenously injected normoglycemic 8-week old male C57Bl6 ApoE-/- mice with normal saline (NS, n = 10) or 25 µg MGO for 10 consecutive weeks (MGOiv, n = 11) with or without 1 g/L pyridoxamine (MGOiv+PD, n = 11) in the drinking water. We measured circulating immune cells by flow cytometry. We quantified aortic arch lesion area in aortic roots after Sudan-black staining. We quantified the expression of inflammatory genes in the aorta by qPCR. Intermittent MGO spikes weekly increased atherosclerotic burden in the arch 1.8-fold (NS: 0.9 ± 0.1 vs 1.6 ± 0.2 %), and this was prevented by pyridoxamine (0.8 ± 0.1 %). MGOiv spikes increased circulating neutrophils and monocytes (2-fold relative to NS) and the expression of ICAM (3-fold), RAGE (5-fold), S100A9 (2-fold) and MCP1 (2-fold). All these changes were attenuated by pyridoxamine. This study suggests that MGO spikes damages the vasculature independently of plasma glucose levels.",
keywords = "Atherosclerosis, Diabetes, Dicarbonyl stress, Methylglyoxal, Pyridoxamine",
author = "Hanssen, {Nordin M. J.} and Chris Tikellis and Pickering, {Raelene J.} and Dragana Dragoljevic and Lee, {Man Kit Sam} and Tomasz Block and Scheijen, {Jean L. JM} and Kristiaan Wouters and Toshio Miyata and Cooper, {Mark E.} and Murphy, {Andrew J.} and Thomas, {Merlin C.} and Schalkwijk, {Casper G.}",
note = "Funding Information: This research is supported by is supported by an E. Dekker grant by the Dutch Heart Foundation (Hartstichting) ( 2017T039 ) and a junior postdoctoral grant from the Dutch Diabetes Foundation (Diabetes Fonds) (2017.85.005. Merlin Thomas is an NHMRC Senior Research Fellow. AJM is supported by National Health and Medical Research Council project grants ( APP1106154 and APP1142938 ). NMJH is supported by a Senior Clinical Dekker grant by the Dutch Heart Foundation (grant number 2021T055 ) and a DFN- DON grant 2020 (Grant number 2020.10.002 ). Publisher Copyright: {\textcopyright} 2023 The Authors",
year = "2023",
month = feb,
day = "1",
doi = "10.1016/j.biopha.2022.114211",
language = "English",
volume = "158",
journal = "Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie",
issn = "0753-3322",
publisher = "Elsevier Masson",

}

RIS

TY - JOUR

T1 - Pyridoxamine prevents increased atherosclerosis by intermittent methylglyoxal spikes in the aortic arches of ApoE-/- mice

AU - Hanssen, Nordin M. J.

AU - Tikellis, Chris

AU - Pickering, Raelene J.

AU - Dragoljevic, Dragana

AU - Lee, Man Kit Sam

AU - Block, Tomasz

AU - Scheijen, Jean L. JM

AU - Wouters, Kristiaan

AU - Miyata, Toshio

AU - Cooper, Mark E.

AU - Murphy, Andrew J.

AU - Thomas, Merlin C.

AU - Schalkwijk, Casper G.

N1 - Funding Information: This research is supported by is supported by an E. Dekker grant by the Dutch Heart Foundation (Hartstichting) ( 2017T039 ) and a junior postdoctoral grant from the Dutch Diabetes Foundation (Diabetes Fonds) (2017.85.005. Merlin Thomas is an NHMRC Senior Research Fellow. AJM is supported by National Health and Medical Research Council project grants ( APP1106154 and APP1142938 ). NMJH is supported by a Senior Clinical Dekker grant by the Dutch Heart Foundation (grant number 2021T055 ) and a DFN- DON grant 2020 (Grant number 2020.10.002 ). Publisher Copyright: © 2023 The Authors

PY - 2023/2/1

Y1 - 2023/2/1

N2 - Methylglyoxal (MGO) is a reactive glucose metabolite linked to diabetic cardiovascular disease (CVD). MGO levels surge during intermittent hyperglycemia. We hypothesize that these MGO spikes contribute to atherosclerosis, and that pyridoxamine as a MGO quencher prevents this injury. To study this, we intravenously injected normoglycemic 8-week old male C57Bl6 ApoE-/- mice with normal saline (NS, n = 10) or 25 µg MGO for 10 consecutive weeks (MGOiv, n = 11) with or without 1 g/L pyridoxamine (MGOiv+PD, n = 11) in the drinking water. We measured circulating immune cells by flow cytometry. We quantified aortic arch lesion area in aortic roots after Sudan-black staining. We quantified the expression of inflammatory genes in the aorta by qPCR. Intermittent MGO spikes weekly increased atherosclerotic burden in the arch 1.8-fold (NS: 0.9 ± 0.1 vs 1.6 ± 0.2 %), and this was prevented by pyridoxamine (0.8 ± 0.1 %). MGOiv spikes increased circulating neutrophils and monocytes (2-fold relative to NS) and the expression of ICAM (3-fold), RAGE (5-fold), S100A9 (2-fold) and MCP1 (2-fold). All these changes were attenuated by pyridoxamine. This study suggests that MGO spikes damages the vasculature independently of plasma glucose levels.

AB - Methylglyoxal (MGO) is a reactive glucose metabolite linked to diabetic cardiovascular disease (CVD). MGO levels surge during intermittent hyperglycemia. We hypothesize that these MGO spikes contribute to atherosclerosis, and that pyridoxamine as a MGO quencher prevents this injury. To study this, we intravenously injected normoglycemic 8-week old male C57Bl6 ApoE-/- mice with normal saline (NS, n = 10) or 25 µg MGO for 10 consecutive weeks (MGOiv, n = 11) with or without 1 g/L pyridoxamine (MGOiv+PD, n = 11) in the drinking water. We measured circulating immune cells by flow cytometry. We quantified aortic arch lesion area in aortic roots after Sudan-black staining. We quantified the expression of inflammatory genes in the aorta by qPCR. Intermittent MGO spikes weekly increased atherosclerotic burden in the arch 1.8-fold (NS: 0.9 ± 0.1 vs 1.6 ± 0.2 %), and this was prevented by pyridoxamine (0.8 ± 0.1 %). MGOiv spikes increased circulating neutrophils and monocytes (2-fold relative to NS) and the expression of ICAM (3-fold), RAGE (5-fold), S100A9 (2-fold) and MCP1 (2-fold). All these changes were attenuated by pyridoxamine. This study suggests that MGO spikes damages the vasculature independently of plasma glucose levels.

KW - Atherosclerosis

KW - Diabetes

KW - Dicarbonyl stress

KW - Methylglyoxal

KW - Pyridoxamine

UR - http://www.scopus.com/inward/record.url?scp=85145743641&partnerID=8YFLogxK

U2 - 10.1016/j.biopha.2022.114211

DO - 10.1016/j.biopha.2022.114211

M3 - Article

C2 - 36916437

VL - 158

JO - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

JF - Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

SN - 0753-3322

M1 - 114211

ER -

ID: 30840384