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. 2002 Oct 7;196(7):887–896. doi: 10.1084/jem.20012044

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Copyright © 2002, The Rockefeller University Press

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Figure 1. — Platelet adhesion to the endothelium of the common carotid artery in ApoE ^−/− mice in vivo. (A) Assessment of platelet adhesion at the carotid bifurcation (lesion-prone-site, A) and within the proximal portion of the common carotid artery. For in vivo microscopy, two imaginary perpendicular axes were dropped through the origin of the internal and the external common carotid artery. Platelet and leukocyte adhesion were determined at high magnification (500-fold) in a 200 × 100 μm area adjacent to a third line, connecting the perpendicular axes at their intersection with the vessel wall (lesion-prone site, A). In a subset of experiments, platelet adhesion was also determined in the proximal portion of the common carotid artery 500 μm upstream of the carotid bifurcation (nonlesion-prone site, B). ACC, common carotid artery; ACE, external carotid artery; ACI, internal carotid artery. (B) Platelet–endothelial cell interactions were investigated in 6-, 8-, 10-, 12-, 16-, and 22-wk-old ApoE ^−/− mice by in vivo fluorescence microscopy of the common carotid artery in situ. Wild-type animals served as controls. The top and bottom panels summarize transient and firm platelet adhesion, respectively, of 10 experiments per group. Platelets were classified according to their interaction with the endothelial cell lining as described previously (reference 5) and are given per mm² of vessel surface. (C) The microphotographs show representative in vivo fluorescence microscopy images at distinct time points. White arrows indicate adherent platelets, and the black arrow indicates the area of a fatty streak. The small inserts demonstrate histological sections of the corresponding carotid artery under investigation (original magnification: 200-fold). Underneath, the in vivo microscopic images representative en face carotid arteries, stained with Sudan III, are given. (D) Assessment of platelet adhesion to lesion-prone (white bars) and nonlesion-prone sites (black bars). Platelet adhesion was quantified in the proximal (nonlesion-prone) carotid artery and adjacent to the carotid bifurcation (lesion-prone) in both, young (10-wk-old) and old (22-wk-old) ApoE ^−/− mice (left). The photomicrograph in the middle shows a representative carotid artery, stained with Sudan III. Atherosclerotic plaque formation occurs preferentially at the carotid bifurcation. Representative histological sections of the carotid bifurcation and the proximal common carotid artery are presented in the right panels (original magnification: 200-fold).

Figure 1. — Platelet adhesion to the endothelium of the common carotid artery in ApoE ^−/− mice in vivo. (A) Assessment of platelet adhesion at the carotid bifurcation (lesion-prone-site, A) and within the proximal portion of the common carotid artery. For in vivo microscopy, two imaginary perpendicular axes were dropped through the origin of the internal and the external common carotid artery. Platelet and leukocyte adhesion were determined at high magnification (500-fold) in a 200 × 100 μm area adjacent to a third line, connecting the perpendicular axes at their intersection with the vessel wall (lesion-prone site, A). In a subset of experiments, platelet adhesion was also determined in the proximal portion of the common carotid artery 500 μm upstream of the carotid bifurcation (nonlesion-prone site, B). ACC, common carotid artery; ACE, external carotid artery; ACI, internal carotid artery. (B) Platelet–endothelial cell interactions were investigated in 6-, 8-, 10-, 12-, 16-, and 22-wk-old ApoE ^−/− mice by in vivo fluorescence microscopy of the common carotid artery in situ. Wild-type animals served as controls. The top and bottom panels summarize transient and firm platelet adhesion, respectively, of 10 experiments per group. Platelets were classified according to their interaction with the endothelial cell lining as described previously (reference 5) and are given per mm² of vessel surface. (C) The microphotographs show representative in vivo fluorescence microscopy images at distinct time points. White arrows indicate adherent platelets, and the black arrow indicates the area of a fatty streak. The small inserts demonstrate histological sections of the corresponding carotid artery under investigation (original magnification: 200-fold). Underneath, the in vivo microscopic images representative en face carotid arteries, stained with Sudan III, are given. (D) Assessment of platelet adhesion to lesion-prone (white bars) and nonlesion-prone sites (black bars). Platelet adhesion was quantified in the proximal (nonlesion-prone) carotid artery and adjacent to the carotid bifurcation (lesion-prone) in both, young (10-wk-old) and old (22-wk-old) ApoE ^−/− mice (left). The photomicrograph in the middle shows a representative carotid artery, stained with Sudan III. Atherosclerotic plaque formation occurs preferentially at the carotid bifurcation. Representative histological sections of the carotid bifurcation and the proximal common carotid artery are presented in the right panels (original magnification: 200-fold).