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. 2009 Feb 27;296(5):H1675–H1682. doi: 10.1152/ajpheart.00665.2008

Fig. 5.

Fig. 5.

Cell surface expression of proinflammatory cell adhesion molecules [vascular cell adhesion molecule (VCAM)-1 (CD106) and intercellular adhesion molecule (ICAM)-1 (CD54)] on EPCs. A: representative flow cytometry histograms of VCAM-1 expression on early EPCs, adult blood-derived late EPCs, and cord blood-derived late EPCs at baseline and with TNF-α stimulation (20 h, 10 ng/ml). All three EPC subtypes express minimal VCAM-1 at baseline; however, only late EPCs show a marked upregulation of VCAM-1, a surface marker characteristic of endothelial inflammation. The quantitative assessment of proinflammatory surface adhesion molecule expression demonstrates that early EPCs upregulate ICAM-1 (C) but not VCAM-1 (B) upon stimulation. Because of the massive response to the stimulation, the mean fluorescence of ICAM-1 and VCAM-1 is shown on the y-axis on a log scale. Late EPCs (both adult and cord blood derived) have a similar response to inflammatory stimulation as mature human aortic endothelial cells (HAECs), thus highlighting their physiological similarity.