Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

Research output: Contribution to journalJournal articleResearchpeer-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 journalJournal articleResearchpeer-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., ... 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 = "4",
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