Figure 6
Figure 6. Inhibition of Hh signaling pathway stimulates neovessel maturation and stability. VEGF-containing (5 µg) pellets in the presence or absence of Smo inhibitor (20 nmol cyclopamine, cyclop) or PDGFR-β inhibitor (20 nmol imatinib) were implanted into the cornea of C3HeB/FeJ mice (n = 8 per group) for 5 days (A) or 28 days (B). ECs were immunostained using anti-CD31 antibody (red, Alexa 564) and MCs with anti-NG2+ antibody (green, Alexa 488). Image capture was performed with Zeiss Observer Z1 microscope (×20). Quantification of total vessel number (C), vessel diameter (D), vessel connections (E), and number of NG2+ cells per vessel (F), 5 days or 28 days after VEGF pellet implantation in the presence (gray histograms) or absence of cyclopamine (black). Data represent means ± SD of relative values vs control corneas. P > .05 (NS); **P < .005; ***P < .0005.

Inhibition of Hh signaling pathway stimulates neovessel maturation and stability. VEGF-containing (5 µg) pellets in the presence or absence of Smo inhibitor (20 nmol cyclopamine, cyclop) or PDGFR-β inhibitor (20 nmol imatinib) were implanted into the cornea of C3HeB/FeJ mice (n = 8 per group) for 5 days (A) or 28 days (B). ECs were immunostained using anti-CD31 antibody (red, Alexa 564) and MCs with anti-NG2+ antibody (green, Alexa 488). Image capture was performed with Zeiss Observer Z1 microscope (×20). Quantification of total vessel number (C), vessel diameter (D), vessel connections (E), and number of NG2+ cells per vessel (F), 5 days or 28 days after VEGF pellet implantation in the presence (gray histograms) or absence of cyclopamine (black). Data represent means ± SD of relative values vs control corneas. P > .05 (NS); **P < .005; ***P < .0005.

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