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Poster Abstract PresentationsSession Title: Poster Session III

Abstract 643: Impaired Integrin β3 Delays Endothelial Cell Regeneration and Contributes to Arteriovenous Graft Failure in mice

Ming Liang, Anlin Liang, Yun Wang, Jin-fei Dong, Ji Du, Jizhong Cheng
Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A643
Ming Liang
Medicine, Baylor College of Medicine, Houston, TX
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Anlin Liang
Medicine, Baylor College of Medicine, Houston, TX
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Yun Wang
Medicine, Baylor College of Medicine, Houston, TX
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Jin-fei Dong
Medicine, Univ of Washington, Seattle, WA
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Ji Du
Beijing Institute of Heart Lung and Blood Vessel Diseases, Beijing Anzhen Hosp Affiliated to the Capital Med Univ,, Beijing, China
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Jizhong Cheng
Medicine, Baylor College of Medicine, Houston, TX
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Abstract

Objective: Neointima formation is associated with stenosis and subsequent thrombosis in arteriovenous grafts (AVG). A role of integrin β3 in the neointima formation of AVGs remains poorly understood.

Approach and Results: In integrin β3-/- mice, we found significantly accelerated occlusion of AVGs compared to the wild type mice. This is caused by the development of neointima and lack of endothelial regeneration. The latter is a direct consequence of impaired functions of circulating angiogenic cells (CACs) and platelets in integrin β3-/- mice. Evidence suggests the involvement of platelet regulating CAC homing to and differentiation at graft sites via TGF-β1 and Notch signaling pathway. First, CACs deficient of integrin β3 impaired adhesion activity toward exposed subendothelium. Second, platelets from integrin β3-/- mice failed to sufficiently stimulate CACs to differentiate into mature endothelial cells. Finally, we found that TGF-β1 level was increased in platelets from integrin β3-/- mice and resulted in enhanced Notch1 activation in CACs in AVGs. These results demonstrate that integrin β3 is critical for endothelial cell homing and differentiation. The increased TGF-β1 and Notch1 signaling mediates integrin β3-/--induced AVG occlusion. This accelerated occlusion of AVGs was reversed in integrin β3-/- mice transplanted with the bone marrow from WT mice.

Conclusion: Our results suggest that boosting integrin β3 function in the endothelial cells and platelets could prevent neointima and thrombosis in AVGs.

  • Endothelial progenitor cell
  • Remodeling
  • Aortocoronary bypass
  • Author Disclosures: M. Liang: None. A. Liang: None. Y. Wang: None. J. Dong: None. J. Du: None. J. Cheng: None.

  • This research has received full or partial funding support from the American Heart Association.

  • © 2015 by American Heart Association, Inc.
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Arteriosclerosis, Thrombosis, and Vascular Biology
May 2015, Volume 35, Issue Suppl 1
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    Abstract 643: Impaired Integrin β3 Delays Endothelial Cell Regeneration and Contributes to Arteriovenous Graft Failure in mice
    Ming Liang, Anlin Liang, Yun Wang, Jin-fei Dong, Ji Du and Jizhong Cheng
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A643, originally published August 11, 2015

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    Abstract 643: Impaired Integrin β3 Delays Endothelial Cell Regeneration and Contributes to Arteriovenous Graft Failure in mice
    Ming Liang, Anlin Liang, Yun Wang, Jin-fei Dong, Ji Du and Jizhong Cheng
    Arteriosclerosis, Thrombosis, and Vascular Biology. 2015;35:A643, originally published August 11, 2015
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