Fig. 5: Effect of netrin-1 on organ-specific EC proliferation.
From: Brain-derived endothelial cells are neuroprotective in a chronic cerebral hypoperfusion mouse model
a 5 × 103 ECs from each organ as indicated were cultured on OP9 feeder cells with several doses of netrin-1 protein and stained with anti-CD31 antibody. Control represents no netrin-1 addition. Representative images are shown on the left. Scale bar, 3 mm. Quantitative evaluation is shown on the right. In each group, values were compared to the no addition of netrin-1 (n = 3 per group). Data are presented as mean ± SEM. b 5 × 103 ECs from each organ as indicated were cultured on OP9 feeder and fetal brain cells, with and without anti–netrin-1 antibody, and stained with anti-CD31 antibody. Representative images are shown on the left. Scale bar, 3 mm. Quantitative evaluation is shown on the right. In each group, values were compared to no addition of brain cells or netrin-1 (n = 3 per group). Data are presented as mean ± SEM. c Quantitative reverse transcription PCR analysis for netrin receptors (Unc 5A, Unc 5B, Unc 5C, Unc 5D, down syndrome cell adhesion molecule [DSCAM], deleted in colorectal cancer [DCC], and neogenin) in ECs from brain, liver, and fat (n = 3 per group). Expression was relative to that of brain ECs. Data are presented as mean ± SEM. d 5 × 103 ECs from each organ as indicated were cultured on OP9 feeder and fetal brain cells, with and without soluble Unc 5B, and stained with anti-CD31 antibody. Representative images are shown on the left. Scale bar, 3 mm. Quantitative evaluation is shown on the right. In each group, values were compared to the no addition of brain cells or soluble UNC5B (n = 3 per group). Data are presented as mean ± SEM. *, P < 0.05; **, P < 0.01; ***, P < 0.001; ns not significant. EC endothelial cell.
