Endothelial cell-selective adhesion molecule modulates atherosclerosis through plaque angiogenesis and monocyte-endothelial interaction

被引：45

作者：

Inoue, Michihiko ^{[1
]}

Ishida, Tatsuro ^{[1
]}

Yasuda, Tomoyuki ^{[1
]}

Toh, Ryuji ^{[1
]}

Hara, Tetsuya ^{[1
]}

Cangara, Husni M. ^{[1
]}

Rikitake, Yoshiyuki ^{[1
]}

Taira, Kazuki ^{[1
]}

Sun, Li ^{[1
]}

Kundu, Ramendra K. ^{[1
]}

Quertermous, Thomas ^{[1
]}

Hirata, Ken-ichi ^{[1
]}

机构：

[1] Kobe Univ, Div Cardiovasc Med, Grad Sch Med, Chuo Ku, Kobe, Hyogo 6500017, Japan

来源：

MICROVASCULAR RESEARCH | 2010年 / 80卷 / 02期

关键词：

Atherosclerosis; Adhesion molecule; Endothelium; Vasa vasorum; Angiogenesis; Monocyte; Macrophage; VASA VASORUM; TRANSENDOTHELIAL MIGRATION; DEFICIENT MICE; IN-VITRO; NEOVASCULARIZATION; EXTRAVASATION; DYSFUNCTION; PROGRESSION; NEUTROPHIL; MECHANISMS;

D O I：

10.1016/j.mvr.2010.04.005

中图分类号：

R6 [外科学];

学科分类号：

1002 ; 100210 ;

摘要：

Endothelial cell-selective adhesion molecule (ESAM) is a new member of the immunoglobulin superfamily, which is expressed in vascular endothelial cells. Previous studies have demonstrated that ESAM regulates angiogenesis, endothelial permeability, and leukocyte transmigration. However, little is known concerning the role of ESAM in atherosclerosis. In this study, we assessed the effects of ESAM inactivation on atherosclerosis in mice. ESAM-/- mice were bred with apoE-/- mice to generate double knockout mice, and the aortic lesion size of apoE-/- and ESAM-/- apoE-/- mice was compared histologically. Although plasma cholesterol levels were higher in ESAM-/- apoE-/- mice, the lesion size was markedly smaller than in apoE-/- mice. ESAM-/- apoE-/- mice exhibited a decrease in the number of vasa vasorum and macrophages in the vessel wall. In vitro adhesion assays showed that THP-1 cells, which did not express ESAM, bound to the ESAM-coated culture plates, suggesting that ESAM may interact with heterophilic ligand(s) on monocytes. Moreover, downregulation of ESAM by siRNA in the endothelial monolayer diminished transendothelial migration of THP-1 cells. In conclusion, ESAM inactivation can reduce susceptibility to atherosclerosis by inhibiting plaque neovascularization and macrophage infiltration into the atheroma. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：179 / 187

页数：9

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