Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

Research output: Contribution to journal › Journal article › Research › peer-review

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Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. / Nobécourt, Estelle; Tabet, Fatiha; Lambert, Gilles; Puranik, Rajesh; Bao, Shisan; Yan, Ling; Davies, Michael Jonathan; Brown, Bronwyn E; Jenkins, Alicia J; Dusting, Gregory J; Bonnet, David J; Curtiss, Linda K; Barter, Philip J; Rye, Kerry-Anne.

In: Arteriosclerosis, Thrombosis, and Vascular Biology, Vol. 30, No. 4, 04.2010, p. 766-72.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Nobécourt, E, Tabet, F, Lambert, G, Puranik, R, Bao, S, Yan, L, Davies, MJ, Brown, BE, Jenkins, AJ, Dusting, GJ, Bonnet, DJ, Curtiss, LK, Barter, PJ & Rye, K-A 2010, 'Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I', Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 30, no. 4, pp. 766-72. https://doi.org/10.1161/ATVBAHA.109.201715

APA

Nobécourt, E., Tabet, F., Lambert, G., Puranik, R., Bao, S., Yan, L., Davies, M. J., Brown, B. E., Jenkins, A. J., Dusting, G. J., Bonnet, D. J., Curtiss, L. K., Barter, P. J., & Rye, K-A. (2010). Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. Arteriosclerosis, Thrombosis, and Vascular Biology, 30(4), 766-72. https://doi.org/10.1161/ATVBAHA.109.201715

Vancouver

Nobécourt E, Tabet F, Lambert G, Puranik R, Bao S, Yan L et al. Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. Arteriosclerosis, Thrombosis, and Vascular Biology. 2010 Apr;30(4):766-72. https://doi.org/10.1161/ATVBAHA.109.201715

Author

Nobécourt, Estelle ; Tabet, Fatiha ; Lambert, Gilles ; Puranik, Rajesh ; Bao, Shisan ; Yan, Ling ; Davies, Michael Jonathan ; Brown, Bronwyn E ; Jenkins, Alicia J ; Dusting, Gregory J ; Bonnet, David J ; Curtiss, Linda K ; Barter, Philip J ; Rye, Kerry-Anne. / Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I. In: Arteriosclerosis, Thrombosis, and Vascular Biology. 2010 ; Vol. 30, No. 4. pp. 766-72.

Bibtex

@article{223c11f28b404a9d840a506701e22475,
title = "Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I",
abstract = "OBJECTIVE: The goal of this study was to investigate the effects of nonenzymatic glycation on the antiinflammatory properties of apolipoprotein (apo) A-I.METHODS AND RESULTS: Rabbits were infused with saline, lipid-free apoA-I from normal subjects (apoA-I(N)), lipid-free apoA-I nonenzymatically glycated by incubation with methylglyoxal (apoA-I(Glyc in vitro)), nonenzymatically glycated lipid-free apoA-I from subjects with diabetes (apoA-I(Glyc in vivo)), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I(N), (A-I(N))rHDL, or apoA-I(Glyc in vitro), (A-I(Glyc in vitro))rHDL. At 24 hours postinfusion, acute vascular inflammation was induced by inserting a nonocclusive, periarterial carotid collar. The animals were euthanized 24 hours after the insertion of the collar. The collars caused intima/media neutrophil infiltration and increased endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). ApoA-I(N) infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-I(Glyc in vitro) infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-I(Glyc in vivo) did not inhibit neutrophil infiltration or adhesion molecule expression. (A-I(Glyc in vitro))rHDL also inhibited vascular inflammation less effectively than (A-I(N))rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-kappaB activation and reactive oxygen species formation.CONCLUSIONS: Nonenzymatic glycation impairs the antiinflammatory properties of apoA-I.",
keywords = "Active Transport, Cell Nucleus, Animals, Anti-Inflammatory Agents, Apolipoprotein A-I, Carotid Arteries, Carotid Artery Injuries, Diabetes Mellitus, Type 2, Diabetic Angiopathies, Disease Models, Animal, Glycosylation, Humans, I-kappa B Proteins, Inflammation, Infusions, Parenteral, Intercellular Adhesion Molecule-1, Lipoproteins, HDL, NF-kappa B, Neutrophil Infiltration, Phosphatidylcholines, Phosphorylation, Protein Processing, Post-Translational, Pyruvaldehyde, Rabbits, Reactive Oxygen Species, Time Factors, Vascular Cell Adhesion Molecule-1",
author = "Estelle Nob{\'e}court and Fatiha Tabet and Gilles Lambert and Rajesh Puranik and Shisan Bao and Ling Yan and Davies, {Michael Jonathan} and Brown, {Bronwyn E} and Jenkins, {Alicia J} and Dusting, {Gregory J} and Bonnet, {David J} and Curtiss, {Linda K} and Barter, {Philip J} and Kerry-Anne Rye",
year = "2010",
month = apr,
doi = "10.1161/ATVBAHA.109.201715",
language = "English",
volume = "30",
pages = "766--72",
journal = "Arteriosclerosis, Thrombosis, and Vascular Biology",
issn = "1079-5642",
publisher = "Lippincott Williams & Wilkins",
number = "4",

}

RIS

TY - JOUR

T1 - Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

AU - Nobécourt, Estelle

AU - Tabet, Fatiha

AU - Lambert, Gilles

AU - Puranik, Rajesh

AU - Bao, Shisan

AU - Yan, Ling

AU - Davies, Michael Jonathan

AU - Brown, Bronwyn E

AU - Jenkins, Alicia J

AU - Dusting, Gregory J

AU - Bonnet, David J

AU - Curtiss, Linda K

AU - Barter, Philip J

AU - Rye, Kerry-Anne

PY - 2010/4

Y1 - 2010/4

N2 - OBJECTIVE: The goal of this study was to investigate the effects of nonenzymatic glycation on the antiinflammatory properties of apolipoprotein (apo) A-I.METHODS AND RESULTS: Rabbits were infused with saline, lipid-free apoA-I from normal subjects (apoA-I(N)), lipid-free apoA-I nonenzymatically glycated by incubation with methylglyoxal (apoA-I(Glyc in vitro)), nonenzymatically glycated lipid-free apoA-I from subjects with diabetes (apoA-I(Glyc in vivo)), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I(N), (A-I(N))rHDL, or apoA-I(Glyc in vitro), (A-I(Glyc in vitro))rHDL. At 24 hours postinfusion, acute vascular inflammation was induced by inserting a nonocclusive, periarterial carotid collar. The animals were euthanized 24 hours after the insertion of the collar. The collars caused intima/media neutrophil infiltration and increased endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). ApoA-I(N) infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-I(Glyc in vitro) infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-I(Glyc in vivo) did not inhibit neutrophil infiltration or adhesion molecule expression. (A-I(Glyc in vitro))rHDL also inhibited vascular inflammation less effectively than (A-I(N))rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-kappaB activation and reactive oxygen species formation.CONCLUSIONS: Nonenzymatic glycation impairs the antiinflammatory properties of apoA-I.

AB - OBJECTIVE: The goal of this study was to investigate the effects of nonenzymatic glycation on the antiinflammatory properties of apolipoprotein (apo) A-I.METHODS AND RESULTS: Rabbits were infused with saline, lipid-free apoA-I from normal subjects (apoA-I(N)), lipid-free apoA-I nonenzymatically glycated by incubation with methylglyoxal (apoA-I(Glyc in vitro)), nonenzymatically glycated lipid-free apoA-I from subjects with diabetes (apoA-I(Glyc in vivo)), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I(N), (A-I(N))rHDL, or apoA-I(Glyc in vitro), (A-I(Glyc in vitro))rHDL. At 24 hours postinfusion, acute vascular inflammation was induced by inserting a nonocclusive, periarterial carotid collar. The animals were euthanized 24 hours after the insertion of the collar. The collars caused intima/media neutrophil infiltration and increased endothelial expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1). ApoA-I(N) infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-I(Glyc in vitro) infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-I(Glyc in vivo) did not inhibit neutrophil infiltration or adhesion molecule expression. (A-I(Glyc in vitro))rHDL also inhibited vascular inflammation less effectively than (A-I(N))rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-kappaB activation and reactive oxygen species formation.CONCLUSIONS: Nonenzymatic glycation impairs the antiinflammatory properties of apoA-I.

KW - Active Transport, Cell Nucleus

KW - Animals

KW - Anti-Inflammatory Agents

KW - Apolipoprotein A-I

KW - Carotid Arteries

KW - Carotid Artery Injuries

KW - Diabetes Mellitus, Type 2

KW - Diabetic Angiopathies

KW - Disease Models, Animal

KW - Glycosylation

KW - Humans

KW - I-kappa B Proteins

KW - Inflammation

KW - Infusions, Parenteral

KW - Intercellular Adhesion Molecule-1

KW - Lipoproteins, HDL

KW - NF-kappa B

KW - Neutrophil Infiltration

KW - Phosphatidylcholines

KW - Phosphorylation

KW - Protein Processing, Post-Translational

KW - Pyruvaldehyde

KW - Rabbits

KW - Reactive Oxygen Species

KW - Time Factors

KW - Vascular Cell Adhesion Molecule-1

U2 - 10.1161/ATVBAHA.109.201715

DO - 10.1161/ATVBAHA.109.201715

M3 - Journal article

C2 - 20110571

VL - 30

SP - 766

EP - 772

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

SN - 1079-5642

IS - 4

ER -

ID: 129670118