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. Author manuscript; available in PMC: 2011 Sep 1.
Published in final edited form as: Hypertension. 2010 Jul 19;56(3):397–404. doi: 10.1161/HYPERTENSIONAHA.110.153262

Figure 2.

Figure 2

(A) Bar graph and representative photomicrographs showing the effects of estradiol (Est; 10nmol/L), PPT (ER-α agonist; 100nmol/L) and DPN (100nmol/L) on capillary formation by EPCs in the presence and absence of the ER-α antagonist MPP (1μmol/L). Serum starved EPCs were plated at a density of 50,000 cells/200μl/well on matrigel coated 8-well multichamber slides. After 4 hours the capillary formation was assessed by microscopically measuring the length of capillaries at 5 random locations (4x-magnification). Values represent means±SEM. (B) EPC-EC were seeded into collagen gels (3.75mg/ml) in EGM2 medium and incubated for 24 hours as follows: (a) control (Cont); (b) VEGF (40ng/ml); (c) estradiol (Est,10nmol/L); or (d), positive control[phorbol myristate actetate (PMA;50ng/ml) + VEGF]. Cultures were subsequently fixed in 2% paraformaldehyde, stained with toluidine blue and photographed. Shown are mean number of lumens and SD; *(P<0.05), **(P<0.01) relative to control, by Student t test. (C) EPC-EC-coated Cytodex3 beads in fibrin gels were cultured in EGM2 medium as follows: (a) without VEGF; (b) with VEGF (15ng/ml); (c) with estradiol (Est,10nmol/L); or (d) with VEGF+E2. Gels were photographed and the number of sprouts counted after 7 days. Shown are means and SD; *(P<0.05), **(P<0.01) relative to control, by Student t test.