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Novel vascular molecule involved in monocyte adhesion to aortic endothelium in models of atherogenesis.

McEvoy LM, Sun H, Tsao PS, Cooke JP, Berliner JA, Butcher EC - J. Exp. Med. (1997)

Bottom Line: VMAP-1 is a 50-kD protein.Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels.VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, Stanford, California 94305, USA.

ABSTRACT
Adhesion of monocytes to the endothelium in lesion-prone areas is one of the earliest events in fatty streak formation leading to atherogenesis. The molecular basis of increased monocyte adhesion is not fully characterized. We have identified a novel vascular monocyte adhesion-associated protein, VMAP-1, that plays a role in adhesion of monocytes to activated endothelium. Originally selected for its ability to block binding of a mouse monocyte-like cell line (WEHI78/24) to cytokine- or LPS-stimulated cultured mouse endothelial cells in vitro, antiVMAP-1 mAb LM151 cross-reacts with rabbit endothelium and blocks binding of human monocytes to cultured rabbit aortic endothelial cells stimulated with minimally modified low density lipoprotein, thought to be a physiologically relevant atherogenic stimulus. Most importantly, LM151 prevents adhesion of normal monocytes and monocytoid cells to intact aortic endothelium from cholesterol-fed rabbits in an ex vivo assay. VMAP-1 is a 50-kD protein. Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels. VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

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VMAP-1 is expressed by arterial and endocardial endothelial cells in vivo. Mouse heart section stained with anti–VMAP-1 mAb LM151 reveals intense reactivity (arrows) with endothelial cells covering valves in the aortic root (A), endocardium lining the ventricle (B), and endothelial cells in  a small artery (C ). No staining was observed with a rat IgM control mAb (OZ42).
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Figure 3: VMAP-1 is expressed by arterial and endocardial endothelial cells in vivo. Mouse heart section stained with anti–VMAP-1 mAb LM151 reveals intense reactivity (arrows) with endothelial cells covering valves in the aortic root (A), endocardium lining the ventricle (B), and endothelial cells in a small artery (C ). No staining was observed with a rat IgM control mAb (OZ42).

Mentions: To ask if VMAP-1 were displayed by aortic and other large vessel endothelium in vivo, frozen sections of heart, kidney, lung, and lymphoid tissues were stained with LM151 or control IgM mAbs MECA79 or OZ42. As illustrated in Fig. 3, anti–VMAP-1 mAb LM151 revealed focal staining of the endothelial lining of valves in the aortic root (Fig. 3 A) and the heart ventricle (Fig. 3 B) as well as of subsets of arteries and arterioles from many tissues including the heart and kidney (Fig. 3 C). No reactivity was observed in capillary endothelium or with postcapillary high endothelial venules in peripheral lymph nodes or PP. VMAP-1 was not restricted to vascular endothelium; LM151 also stained subsets of bronchial and intestinal epithelial cells and stromal elements in lymphoid tissues, but did not stain any leukocytes (lymphocytes, monocytes, and neutrophils) isolated from lymph nodes, spleen, or bone marrow, as assessed by FACS® analysis (not shown).


Novel vascular molecule involved in monocyte adhesion to aortic endothelium in models of atherogenesis.

McEvoy LM, Sun H, Tsao PS, Cooke JP, Berliner JA, Butcher EC - J. Exp. Med. (1997)

VMAP-1 is expressed by arterial and endocardial endothelial cells in vivo. Mouse heart section stained with anti–VMAP-1 mAb LM151 reveals intense reactivity (arrows) with endothelial cells covering valves in the aortic root (A), endocardium lining the ventricle (B), and endothelial cells in  a small artery (C ). No staining was observed with a rat IgM control mAb (OZ42).
© Copyright Policy
Related In: Results  -  Collection

Show All Figures
getmorefigures.php?uid=PMC2196357&req=5

Figure 3: VMAP-1 is expressed by arterial and endocardial endothelial cells in vivo. Mouse heart section stained with anti–VMAP-1 mAb LM151 reveals intense reactivity (arrows) with endothelial cells covering valves in the aortic root (A), endocardium lining the ventricle (B), and endothelial cells in a small artery (C ). No staining was observed with a rat IgM control mAb (OZ42).
Mentions: To ask if VMAP-1 were displayed by aortic and other large vessel endothelium in vivo, frozen sections of heart, kidney, lung, and lymphoid tissues were stained with LM151 or control IgM mAbs MECA79 or OZ42. As illustrated in Fig. 3, anti–VMAP-1 mAb LM151 revealed focal staining of the endothelial lining of valves in the aortic root (Fig. 3 A) and the heart ventricle (Fig. 3 B) as well as of subsets of arteries and arterioles from many tissues including the heart and kidney (Fig. 3 C). No reactivity was observed in capillary endothelium or with postcapillary high endothelial venules in peripheral lymph nodes or PP. VMAP-1 was not restricted to vascular endothelium; LM151 also stained subsets of bronchial and intestinal epithelial cells and stromal elements in lymphoid tissues, but did not stain any leukocytes (lymphocytes, monocytes, and neutrophils) isolated from lymph nodes, spleen, or bone marrow, as assessed by FACS® analysis (not shown).

Bottom Line: VMAP-1 is a 50-kD protein.Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels.VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

View Article: PubMed Central - PubMed

Affiliation: Laboratory of Immunology and Vascular Biology, Department of Pathology, Stanford University, Stanford, California 94305, USA.

ABSTRACT
Adhesion of monocytes to the endothelium in lesion-prone areas is one of the earliest events in fatty streak formation leading to atherogenesis. The molecular basis of increased monocyte adhesion is not fully characterized. We have identified a novel vascular monocyte adhesion-associated protein, VMAP-1, that plays a role in adhesion of monocytes to activated endothelium. Originally selected for its ability to block binding of a mouse monocyte-like cell line (WEHI78/24) to cytokine- or LPS-stimulated cultured mouse endothelial cells in vitro, antiVMAP-1 mAb LM151 cross-reacts with rabbit endothelium and blocks binding of human monocytes to cultured rabbit aortic endothelial cells stimulated with minimally modified low density lipoprotein, thought to be a physiologically relevant atherogenic stimulus. Most importantly, LM151 prevents adhesion of normal monocytes and monocytoid cells to intact aortic endothelium from cholesterol-fed rabbits in an ex vivo assay. VMAP-1 is a 50-kD protein. Immunohistology of vessels reveals focal constitutive expression in aorta and other large vessels. VMAP-1 is thus a novel vascular adhesion-associated protein that appears to play a critical role in monocyte adhesion to aortic endothelial cells in atherogenesis in vivo.

Show MeSH
Related in: MedlinePlus