Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

Estelle Nobécourt; Fatiha Tabet; Gilles Lambert; Rajesh Puranik; Shisan Bao; Ling Yan; Michael Jonathan Davies; Bronwyn E Brown; Alicia J Jenkins; Gregory J Dusting; David J Bonnet; Linda K Curtiss; Philip J Barter; Kerry-Anne Rye

doi:10.1161/ATVBAHA.109.201715

Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

Estelle Nobécourt, Fatiha Tabet, Gilles Lambert, Rajesh Puranik, Shisan Bao, Ling Yan, Michael Jonathan Davies, Bronwyn E Brown, Alicia J Jenkins, Gregory J Dusting, David J Bonnet, Linda K Curtiss, Philip J Barter, Kerry-Anne Rye

92 Citations (Scopus)

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-IN)rHDL, or apoA-IGlyc 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-IGlyc in vitro infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-IGlyc 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-IN)rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-κB activation and reactive oxygen species formation. Conclusion: Nonenzymatic glycation impairs the antiinflammatory properties of apoA-I.

Original language	English
Journal	Arteriosclerosis, Thrombosis, and Vascular Biology
Volume	30
Issue number	4
Pages (from-to)	766-72
Number of pages	7
ISSN	1079-5642
DOIs	https://doi.org/10.1161/ATVBAHA.109.201715
Publication status	Published - Apr 2010
Externally published	Yes

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

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.1161/ATVBAHA.109.201715

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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

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

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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-IN), 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-IGlyc in vivo), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I N, (A-IN)rHDL, or apoA-IGlyc 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-IN infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-IGlyc in vitro infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-IGlyc in vivo did not inhibit neutrophil infiltration or adhesion molecule expression. (A-IGlyc in vitro)rHDL also inhibited vascular inflammation less effectively than (A-IN)rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-κB activation and reactive oxygen species formation. Conclusion: 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",

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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-IN), 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-IGlyc in vivo), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I N, (A-IN)rHDL, or apoA-IGlyc 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-IN infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-IGlyc in vitro infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-IGlyc in vivo did not inhibit neutrophil infiltration or adhesion molecule expression. (A-IGlyc in vitro)rHDL also inhibited vascular inflammation less effectively than (A-IN)rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-κB activation and reactive oxygen species formation. Conclusion: 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-IN), 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-IGlyc in vivo), discoidal reconstituted high-density lipoproteins (rHDL) containing phosphatidylcholine and apoA-I N, (A-IN)rHDL, or apoA-IGlyc 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-IN infusion decreased neutrophil infiltration and VCAM-1 and ICAM-1 expression by 89%, 90%, and 66%, respectively. The apoA-IGlyc in vitro infusion decreased neutrophil infiltration by 53% but did not reduce VCAM-1 or ICAM-1 expression. ApoA-IGlyc in vivo did not inhibit neutrophil infiltration or adhesion molecule expression. (A-IGlyc in vitro)rHDL also inhibited vascular inflammation less effectively than (A-IN)rHDL. The reduced antiinflammatory properties of nonenzymatically glycated apoA-I were attributed to a reduced ability to inhibit nuclear factor-κB activation and reactive oxygen species formation. Conclusion: 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

SN - 1079-5642

VL - 30

SP - 766

EP - 772

JO - Arteriosclerosis, Thrombosis, and Vascular Biology

JF - Arteriosclerosis, Thrombosis, and Vascular Biology

IS - 4

ER -

Nonenzymatic glycation impairs the antiinflammatory properties of apolipoprotein A-I

Abstract

Keywords

UN SDGs

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