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Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice

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Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice. / Brill, Alexander; Yesilaltay, Ayce; De Meyer, Simon F; Kisucka, Janka; Fuchs, Tobias A; Kocher, Olivier; Krieger, Monty; Wagner, Denisa D.

In: ARTERIOSCL THROM VAS, Vol. 32, No. 8, 01.08.2012, p. 1841-7.

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

Harvard

Brill, A, Yesilaltay, A, De Meyer, SF, Kisucka, J, Fuchs, TA, Kocher, O, Krieger, M & Wagner, DD 2012, 'Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice', ARTERIOSCL THROM VAS, vol. 32, no. 8, pp. 1841-7. https://doi.org/10.1161/ATVBAHA.112.252130

APA

Brill, A., Yesilaltay, A., De Meyer, S. F., Kisucka, J., Fuchs, T. A., Kocher, O., Krieger, M., & Wagner, D. D. (2012). Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice. ARTERIOSCL THROM VAS, 32(8), 1841-7. https://doi.org/10.1161/ATVBAHA.112.252130

Vancouver

Brill A, Yesilaltay A, De Meyer SF, Kisucka J, Fuchs TA, Kocher O et al. Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice. ARTERIOSCL THROM VAS. 2012 Aug 1;32(8):1841-7. https://doi.org/10.1161/ATVBAHA.112.252130

Bibtex

@article{4dfc2087064c4997ac723b9e1a78304e,
title = "Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice",
abstract = "OBJECTIVE: Deep vein thrombosis (DVT) and pulmonary embolism are frequent causes of morbidity and mortality. The goal of our study was to determine whether plasma high-density lipoprotein (HDL), which inversely correlates with the risk of cardiovascular events, affects DVT.METHODS AND RESULTS: Using a murine DVT model of inferior vena cava stenosis, we demonstrated that deficiency of the HDL receptor, scavenger receptor class B type I (SR-BI), promotes venous thrombosis. As SR-BI(-/-) mice have increased plasma cholesterol levels and abnormal HDL particles, we tested SR-BI(-/-) mice with an SR-BI liver transgene that normalizes both parameters. These mice also exhibited increased susceptibility to DVT, indicating a protective role of extrahepatic SR-BI. Mice lacking the major HDL apolipoprotein apoA-I or endothelial nitric oxide synthase (eNOS) (a downstream target of endothelial SR-BI signaling) also had a prothrombotic phenotype. Intravenous infusion of human apoA-I, an HDL component and SR-BI ligend, prevented DVT in wild-type but not SR-BI(-/-) or eNOS(-/-) mice, suggesting that its effect is mediated by SR-BI and eNOS. Intravenous apoA-I infusion abolished histamine-induced platelet-endothelial interactions, which are important for DVT initiation.CONCLUSIONS: An apoA-I (HDL)-SR-BI-eNOS axis is highly protective in DVT and may provide new targets for prophylaxis and treatment of venous thrombosis.",
keywords = "Animals, Apolipoprotein A-I, Blood Coagulation, Blood Platelets, Female, Male, Mice, Mice, Inbred C57BL, Nitric Oxide Synthase Type III, Scavenger Receptors, Class B, Venous Thrombosis",
author = "Alexander Brill and Ayce Yesilaltay and {De Meyer}, {Simon F} and Janka Kisucka and Fuchs, {Tobias A} and Olivier Kocher and Monty Krieger and Wagner, {Denisa D}",
year = "2012",
month = aug,
day = "1",
doi = "10.1161/ATVBAHA.112.252130",
language = "English",
volume = "32",
pages = "1841--7",
journal = "ARTERIOSCL THROM VAS",
issn = "1079-5642",
publisher = "Lippincott Williams and Wilkins",
number = "8",

}

RIS

TY - JOUR

T1 - Extrahepatic high-density lipoprotein receptor SR-BI and apoA-I protect against deep vein thrombosis in mice

AU - Brill, Alexander

AU - Yesilaltay, Ayce

AU - De Meyer, Simon F

AU - Kisucka, Janka

AU - Fuchs, Tobias A

AU - Kocher, Olivier

AU - Krieger, Monty

AU - Wagner, Denisa D

PY - 2012/8/1

Y1 - 2012/8/1

N2 - OBJECTIVE: Deep vein thrombosis (DVT) and pulmonary embolism are frequent causes of morbidity and mortality. The goal of our study was to determine whether plasma high-density lipoprotein (HDL), which inversely correlates with the risk of cardiovascular events, affects DVT.METHODS AND RESULTS: Using a murine DVT model of inferior vena cava stenosis, we demonstrated that deficiency of the HDL receptor, scavenger receptor class B type I (SR-BI), promotes venous thrombosis. As SR-BI(-/-) mice have increased plasma cholesterol levels and abnormal HDL particles, we tested SR-BI(-/-) mice with an SR-BI liver transgene that normalizes both parameters. These mice also exhibited increased susceptibility to DVT, indicating a protective role of extrahepatic SR-BI. Mice lacking the major HDL apolipoprotein apoA-I or endothelial nitric oxide synthase (eNOS) (a downstream target of endothelial SR-BI signaling) also had a prothrombotic phenotype. Intravenous infusion of human apoA-I, an HDL component and SR-BI ligend, prevented DVT in wild-type but not SR-BI(-/-) or eNOS(-/-) mice, suggesting that its effect is mediated by SR-BI and eNOS. Intravenous apoA-I infusion abolished histamine-induced platelet-endothelial interactions, which are important for DVT initiation.CONCLUSIONS: An apoA-I (HDL)-SR-BI-eNOS axis is highly protective in DVT and may provide new targets for prophylaxis and treatment of venous thrombosis.

AB - OBJECTIVE: Deep vein thrombosis (DVT) and pulmonary embolism are frequent causes of morbidity and mortality. The goal of our study was to determine whether plasma high-density lipoprotein (HDL), which inversely correlates with the risk of cardiovascular events, affects DVT.METHODS AND RESULTS: Using a murine DVT model of inferior vena cava stenosis, we demonstrated that deficiency of the HDL receptor, scavenger receptor class B type I (SR-BI), promotes venous thrombosis. As SR-BI(-/-) mice have increased plasma cholesterol levels and abnormal HDL particles, we tested SR-BI(-/-) mice with an SR-BI liver transgene that normalizes both parameters. These mice also exhibited increased susceptibility to DVT, indicating a protective role of extrahepatic SR-BI. Mice lacking the major HDL apolipoprotein apoA-I or endothelial nitric oxide synthase (eNOS) (a downstream target of endothelial SR-BI signaling) also had a prothrombotic phenotype. Intravenous infusion of human apoA-I, an HDL component and SR-BI ligend, prevented DVT in wild-type but not SR-BI(-/-) or eNOS(-/-) mice, suggesting that its effect is mediated by SR-BI and eNOS. Intravenous apoA-I infusion abolished histamine-induced platelet-endothelial interactions, which are important for DVT initiation.CONCLUSIONS: An apoA-I (HDL)-SR-BI-eNOS axis is highly protective in DVT and may provide new targets for prophylaxis and treatment of venous thrombosis.

KW - Animals

KW - Apolipoprotein A-I

KW - Blood Coagulation

KW - Blood Platelets

KW - Female

KW - Male

KW - Mice

KW - Mice, Inbred C57BL

KW - Nitric Oxide Synthase Type III

KW - Scavenger Receptors, Class B

KW - Venous Thrombosis

U2 - 10.1161/ATVBAHA.112.252130

DO - 10.1161/ATVBAHA.112.252130

M3 - SCORING: Journal article

C2 - 22652597

VL - 32

SP - 1841

EP - 1847

JO - ARTERIOSCL THROM VAS

JF - ARTERIOSCL THROM VAS

SN - 1079-5642

IS - 8

ER -