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Figure 1 | Cell Communication and Signaling

Figure 1

From: Slit2N and Robo4 regulate lymphangiogenesis through the VEGF-C/VEGFR-3 pathway

Figure 1

Slit2N inhibits VEGF-C-enhanced growth, migration and tube formation of L-LECs. (A) Proliferation of L-LECs as assessed by MTS assay after incubation with control, 10 nM Slit2N, or VEGF-C [100 ng/ml]; or after preincubation with Slit2N, then VEGF-C. Data represent the mean ± SD of 3 independent experiments (*p < 0.05). (B) Transwell migration of L-LECs after treatment with control, 10 nM Slit2N, or VEGF-C [100 ng/ml]; or after preincubation with Slit2N, then VEGF-C. Data represent the mean ± SD of 3 independent experiments (***p < 0.001). (C) Representative tube formation assay on ECM of L-LECs after treatment with control, 10 nM Slit2N, or VEGF-C [100 ng/ml]; or after preincubation with Slit2N, then VEGF-C. (D) Average length of L-LEC tubes as assessed by in vitro tube formation assay on ECM after treatment with 10 nM Slit2N, VEGF-C [100 ng/ml]; or after preincubation with Slit2N, then VEGF-C, relative to average tube length of untreated cells (Slit2N “-”, VEGF-C “-”). Data represent the mean ± SD of 3 independent experiments (*p < 0.05). (E) Representative Western blot analysis of Slit2N expression in L-LECs transduced with a control adenovirus (Ctrl) or with an adenovirus expressing V5-tagged Slit2N. GAPDH used as loading control. (F) Average length of L-LEC tubes in L-LECs transduced with a control adenovirus (Slit2N-Adenovirus “-”) or in L-LECs transduced with a Slit2N-expressing adenovirus (Slit2N-Adenovirus “+”) as assessed by in vitro tube formation assay on ECM after incubation with control (VEGF-C “-”) or with VEGF-C [100 ng/ml] (VEGF-C “+”), relative to average tube length of untreated L-LECs transduced with control adenovirus (Slit2N-Adenovirus “-”, VEGF-C “-”). Data represent the mean ± SD of 3 independent experiments (***p < 0.001).

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