GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation

James L. Park; Charles W. Heilig; Frank C. Brosius

doi:10.1016/j.ejphar.2004.06.022

GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation

James L. Park, Charles W. Heilig, Frank C. Brosius

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

10 Scopus citations

Abstract

We tested the hypothesis that decreased glucose transporter 1 (GLUT1) expression alters endothelial function. Nitric oxide-dependent endothelial relaxation, but not endothelium-independent relaxation, was significantly reduced in aortas from transgenic mice expressing GLUT1 antisense mRNA, compared to aortas from nontransgenic littermates. These data suggest that GLUT1-dependent glucose metabolism may play an important role in regulating endothelial function.

Original language	English (US)
Pages (from-to)	213-214
Number of pages	2
Journal	European Journal of Pharmacology
Volume	496
Issue number	1
DOIs	https://doi.org/10.1016/j.ejphar.2004.06.022
State	Published - Aug 2 2004
Externally published	Yes

Keywords

Antisense
Endothelium
GLUT1 (glucose transporter1)

ASJC Scopus subject areas

Pharmacology

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10.1016/j.ejphar.2004.06.022

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title = "GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation",

abstract = "We tested the hypothesis that decreased glucose transporter 1 (GLUT1) expression alters endothelial function. Nitric oxide-dependent endothelial relaxation, but not endothelium-independent relaxation, was significantly reduced in aortas from transgenic mice expressing GLUT1 antisense mRNA, compared to aortas from nontransgenic littermates. These data suggest that GLUT1-dependent glucose metabolism may play an important role in regulating endothelial function.",

keywords = "Antisense, Endothelium, GLUT1 (glucose transporter1)",

author = "Park, {James L.} and Heilig, {Charles W.} and Brosius, {Frank C.}",

note = "Funding Information: This work was supported by NIH Grants HL65667 and HL60156 to FCB and an institutional NIH postdoctoral fellowship, T32 HL07853 (Training in Molecular and Cellular Cardiology), to JLP.",

year = "2004",

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doi = "10.1016/j.ejphar.2004.06.022",

language = "English (US)",

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pages = "213--214",

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T1 - GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation

AU - Park, James L.

AU - Heilig, Charles W.

AU - Brosius, Frank C.

N1 - Funding Information: This work was supported by NIH Grants HL65667 and HL60156 to FCB and an institutional NIH postdoctoral fellowship, T32 HL07853 (Training in Molecular and Cellular Cardiology), to JLP.

PY - 2004/8/2

Y1 - 2004/8/2

N2 - We tested the hypothesis that decreased glucose transporter 1 (GLUT1) expression alters endothelial function. Nitric oxide-dependent endothelial relaxation, but not endothelium-independent relaxation, was significantly reduced in aortas from transgenic mice expressing GLUT1 antisense mRNA, compared to aortas from nontransgenic littermates. These data suggest that GLUT1-dependent glucose metabolism may play an important role in regulating endothelial function.

AB - We tested the hypothesis that decreased glucose transporter 1 (GLUT1) expression alters endothelial function. Nitric oxide-dependent endothelial relaxation, but not endothelium-independent relaxation, was significantly reduced in aortas from transgenic mice expressing GLUT1 antisense mRNA, compared to aortas from nontransgenic littermates. These data suggest that GLUT1-dependent glucose metabolism may play an important role in regulating endothelial function.

KW - Antisense

KW - Endothelium

KW - GLUT1 (glucose transporter1)

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VL - 496

SP - 213

EP - 214

JO - European Journal of Pharmacology

JF - European Journal of Pharmacology

SN - 0014-2999

IS - 1

ER -

GLUT1-deficient mice exhibit impaired endothelium-dependent vascular relaxation

Abstract

Keywords

ASJC Scopus subject areas

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