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. Author manuscript; available in PMC: 2012 Mar 1.
Published in final edited form as: Clin Cancer Res. 2011 Mar 1;17(5):1044–1056. doi: 10.1158/1078-0432.CCR-10-2241

Figure 1.

Figure 1

rFKBPL protein inhibits angiogenesis in vitro and ex vivo (A) Transient transfection of an FKBPL cDNA construct inhibits migration of wounded HMEC-1 monolayers compared to empty vector controls. Representative images of wounded monolayers and overexpression of FKBPL following transfection. The histogram shows the wound size relative to wound size at time=0 h ± SEM; n=3. Significance was determined by ANOVA. (B) Inhibition of HMEC-1 wound closure (compared to time matched control) after exposure to a range of concentrations of rFKBPL. Data points show means ± SEM; n=3. (C) Inhibition of HMEC-1 tubule formation in matrigel following exposure to increasing concentrations of rFKBPL; data are corrected to a sham treated control. Data points are means ± SEM; n=3. (D) Microvessel sprouting from rat aortic rings incubated with increasing concentrations of rFKBPL (left panel). Quantitative determination of vessel length and number of vessels after 7 days compared to time matched controls (right panel). Data points are means ± SEM; n=3.