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Angiopoietin-1 promotes atherosclerosis by increasing the proportion of circulating Gr1+ monocytes

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Original languageEnglish
JournalCardiovascular Research
Volume113
Issue number1
DOIs
Publication statusPublished - 9 Jan 2017

Abstract

Aims Atherosclerosis is a chronic inflammatory disease occurring within the
artery wall. A crucial step in atherogenesis is the infiltration and retention of
monocytes into the subendothelial space of large arteries induced by
chemokines and growth factors. Angiopoietin-1 (Ang-1) regulates
angiogenesis and reduces vascular permeability and has also been reported to
promote monocyte migration in vitro. We investigated the role of Ang-1 in
atherosclerosis-prone apolipoprotein-E (ApoE) knockout mouse.
Methods and Results Apo-E knockout (Apo-E-/-) mice fed a Western or
normal chow diet received a single i.v. injection of adenovirus encoding Ang-1
or control vector. Adenovirus-mediated systemic expression of Ang-1 induced
a significant increase in early atherosclerotic lesion size and
monocyte/macrophage accumulation compared with control animals receiving
empty vector. Ang-1 significantly increased plasma MCP-1 and VEGF levels
as measured by ELISA. FACS analysis showed that Ang-1 selectively
increased inflammatory Gr1+ monocytes in the circulation, while the cellsurface
expression of CD11b, which mediates monocyte emigration, was
significantly reduced.
Conclusions Ang-1 specifically increases circulating Gr1+ inflammatory
monocytes and increases monocyte/macrophage retention in atherosclerotic
plaques, thereby contributing to development of atherosclerosis.

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