Figure 3. The PLXDC2 dependence of PEDF's effect on endothelial cell SVEC4-10.
(A) PEDF promoted-cell death of SVEC4-10 cells is suppressed by siRNA-mediated knockdown of PLXDC2, but not PLXDC1. Survival of control siRNA tranfected cells without PEDF treatment is defined as 1. Statistical significance is shown on the top. ** = p < 0.01, and NS = not significant. (B) Left panel: Schematic diagrams of full length receptors and the fusion proteins for the receptor cytoplasmic tails. The cytoplasmic tail of the receptor is fused to the TM domain of DCC, which is fused to the secretion signal of alkaline phosphase at the N-terminus. Alignment of human, mouse, rat and bovine PLXDC2 cytoplasmic tails shows complete conservation (bottom). Locations of potential phosphorylation sites are indicated. Right panel: Expression of cytoplasmic tail of PLXDC2, but not the cytoplasmic tail of PLXDC1 promotes SVEC4-10 cell death. PLXDC2 double mutant S506A/Y511F has greater activity. Survival of control EGFP transfected cells without PEDF treatment is defined as 1. Statistical significance of the comparison of cells without PEDF treatment (with the control cells without PEDF treatment) is shown in blue. Statistical significance of the comparison of cells with PEDF treatment (with the control cells with PEDF treatment) is shown in red. * = p < 0.05, ** = p < 0.01, and NS = not significant.
Figure 3—figure supplement 1. Unbiased screening for effective siRNAs that knock down PLXDC1 or PLXDC2 expression in endothelial cell SVEC4-10.
