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Heyu Ni, Cécile V. Denis, Sangeetha Subbarao, Jay L. Degen, Thomas N. Sato, Richard O. Hynes, Denisa D. Wagner
Published in Volume 106, Issue 3
J Clin Invest. 2000; 106(3):385–392 doi:10.1172/JCI9896
Abstract | Full text | PDF
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Figure 1

Arteriolar injury and denudation of endothelium induced by FeCl3. (a) Progression of FeCl3-induced injury. Fluorescence intensity of endothelium of mesenteric arterioles (n = 14/group) from GFP-transgenic mice was blindly ranked from 5 to 0. FeCl3-treated or untreated arterioles were then compared by Mann-Whitney U test. Before FeCl3 treatment (0 min), all arterioles had a similar intensity (∼5). Significant differences were found after 1 minute of FeCl3 exposure (P = 0.0006). After 2 minutes (not shown), the intensity in control vessels decreased only slightly (mean = 4.1), whereas in FeCl3-treated vessels, fluorescence was greatly decreased (mean = 1.4; P = 0.0001). After 4 minutes, the fluorescence intensity in the control group was still high (mean = 3.4), but in the FeCl3 group was almost undetectable (mean = 0.4; P < 0.0001). Representative photographs of one vessel from each group are shown. (b) Denudation of endothelium by FeCl3. Control (∼130 μm diameter) and FeCl3-treated (∼100 μm diameter) sections of mesenteric arterioles from wild-type mice were stained with rabbit anti-human vWF polyclonal Ab, which cross-reacts with mouse vWF. Endothelial cells in the control arteriole were heavily stained, whereas only a few areas were stained with this Ab (arrow) after 5-minute FeCl3 treatment. These areas may be remaining endothelial cells or small thrombi. The brown ring at the inner side of the injured vessel wall may result from plasma vWF deposition or from subendothelial vWF.