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Increased atherosclerosis in mice with vascular ATP-binding cassette transporter G1 deficiency--brief report

Westerterp, M., Koetsveld, J., Yu, S., Han, S., Li, R., Goldberg, I. J., Welch, C. L. & Tall, A. R., Nov-2010, In : Arteriosclerosis, thrombosis, and vascular biology. 30, 11, p. 2103-2105 3 p.

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  • Increased Atherosclerosis in Mice With Vascular ATP-Binding Cassette Transporter G1 Deficiency—Brief Report

    Final publisher's version, 187 KB, PDF-document

DOI

  • Marit Westerterp
  • Joris Koetsveld
  • Shuiqing Yu
  • Seongah Han
  • Rong Li
  • Ira J Goldberg
  • Carrie L Welch
  • Alan R Tall

OBJECTIVE: The objective of this study was to investigate the role of vascular ATP-binding cassette transporter G1 (ABCG1) in atherogenesis without a confounding difference in macrophage ABCG1 expression. ABCG1 is highly expressed in macrophages and endothelial cells. ABCG1 preserves endothelial function by maintaining endothelial NO synthase activity and by reducing adhesion molecule expression and monocyte adhesion.

METHODS AND RESULTS: To investigate the role of vascular ABCG1 in atherosclerosis in vivo Abcg1(-/-)/Ldlr(-/-) and Ldlr(-/-) mice were transplanted with wild-type bone marrow and fed a Western-type diet for 12 or 23 weeks. The atherosclerotic lesion area was similar in both groups after 12 weeks but was increased in Abcg1(-/-)/Ldlr(-/-) recipients after 23 weeks, especially in the aortic arch (2.2-fold; P<0.01). Endothelial NO synthase-mediated vascular relaxation was impaired in male Abcg1(-/-)/Ldlr(-/-) recipients.

CONCLUSIONS: Our data show an atheroprotective role of vascular ABCG1, especially in the aortic arch, likely related to its role in the preservation of endothelial NO synthase activity.

Original languageEnglish
Pages (from-to)2103-2105
Number of pages3
JournalArteriosclerosis, thrombosis, and vascular biology
Volume30
Issue number11
Publication statusPublished - Nov-2010

    Keywords

  • ATP Binding Cassette Transporter, Subfamily G, Member 1, ATP-Binding Cassette Transporters/metabolism, Animals, Aorta/metabolism, Atherosclerosis/metabolism, Disease Models, Animal, Lipoproteins/deficiency, Mice

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