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. 2011 Nov 11;287(1):408–417. doi: 10.1074/jbc.M111.261818

FIGURE 5.

FIGURE 5.

PI3K and eNOS contribute to omentin-induced endothelial cell responses. A, contribution of PI3K and eNOS to omentin-mediated endothelial cell differentiation. HUVECs were pretreated with LY294002 (50 μmol/liter), l-NAME (1 mmol/liter), or vehicle (dimethyl sulfoxide) and treated with omentin (300 ng/ml) or vehicle for 18 h. A Matrigel assay was performed. Quantitative analyses of the network tube length are shown. Results are shown as the mean ± S.D. (n = 5). B and C, PI3K and eNOS participate in omentin-induced endothelial cell survival. After treatment with LY294002 (50 μmol/liter), l-NAME (1 mmol/liter) or vehicle (dimethyl sulfoxide), cells were treated with omentin (300 ng/ml) or vehicle followed by 48 h of incubation with serum-free media. Apoptotic nuclei were identified by TUNEL staining, and total nuclei were identified by 4′,6-diamidino-2-phenylindole counterstaining (B). Quantitative analyses of the frequency of TUNEL-positive HUVECs are shown. Nucleosome fragmentation was assessed by enzyme-linked immunosorbent assay (C). Results are shown as the mean ± S.D. (n = 5).