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. 2012 Sep 13;61(10):2621–2632. doi: 10.2337/db11-1768

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© 2012 by the American Diabetes Association.

Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered. See http://creativecommons.org/licenses/by-nc-nd/3.0/ for details.

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FIG. 5. — Effects of EFNB2 stimulation on diabetic PB-MNCs. A: Effects of specific inhibitor of PI 3-kinase signaling pathway (LY29004) on the adhesion of untreated (upper panel) (n = 4–10 per group) or pretreated (lower panel) (n = 5–10 per group) PB-MNCs from diabetic patients. B: Effects of specific inhibitor of MEK-1/2 signaling pathway (PD98059) on the adhesion ability of control (upper panel) (n = 5 per group) or pretreated (lower panel) (n = 5 per group) PB-MNCs from diabetic patients. C: Role of EFNB2 stimulation on the migration of PB-MNCs from diabetic patients (n = 12 per group). D: Representative images of capillary-like tube formation in cocultures of HUVECs and nonpretreated (upper panel) or pretreated (lower panel) diabetic PB-MNCs. E: Representative images of incorporated EFNB2-pretreated diabetic PB-MNCs (green) in the HUVEC network (red). F: Quantitative analysis of HUVEC network formation: intersection number, length, and surface (n = 9). NS, nonstimulated; Diab, diabetic. *P < 0.05; **P < 0.01; ***P < 0.001. (A high-quality digital representation of this figure is available in the online issue.)