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. Author manuscript; available in PMC: 2019 May 1.
Published in final edited form as: Angiogenesis. 2018 Jan 11;21(2):215–228. doi: 10.1007/s10456-017-9589-y

Fig. 6. VEGF and IL-8 produced from IL-11 treated RA ST fibroblasts, contribute to the indirect effect of IL-11 on angiogenesis.

Fig. 6

A. RA ST fibroblasts were either untreated (PBS) or stimulated with IL-11 (100ng/ml) for 48h and concentration of IL-8, VEGF, Ang1, CXCL1 and CXCL5 was determined by ELISA. B. Representative images of HUVECs that migrated in response to supernatants from RA ST fibroblasts that were untreated (PBS sup) or treated for 48h with IL-11 (100ng/ml). IL-11Rα-Fc chimera (10μg/ml) was incubated for 1h with the collected supernatants. C. Number of the HUVECs that migrated in different treatment groups shown in B. D. Endothelial tube formation assay was performed (18h) in response to supernatants from RA ST fibroblasts that were untreated (PBS sup) or treated with IL-11 (100ng/ml) for 48h, while HUVECs were preincubated with 10μg/ml of IgG, anti-CXCR1, anti-VEGFR2, anti-CXCR1 plus anti-VEGFR2 Abs. All the experiments were performed in triplicate and repeated three times, n=3. E. The branching points were counted in each treatment condition in D. F. RA PB in vitro differentiated macrophages were untreated (PBS) or stimulated with IL-11 (100ng/ml) for 48h and the supernatant levels of IL-6 and CCL2 were determined by ELISA, n=5. Values are the mean ± SD. * represents p <0.05.