Fig. 3
From: Blocking Jak/STAT signalling using tofacitinib inhibits angiogenesis in experimental arthritis
Effect of tofacitinib on chemoinvasion and proliferation of HC-ECs. (A) The histogram showed the median and the range of migrated HC-ECs. VEGF (20 ng/ml) significantly induced an increase of number of migrated HC-ECs, when compared untreated (UT) HC-ECs and the treatment with 1 μM of tofacitinib significantly decrease the effects of VEGF (**p = 0.007). (B)The histogram showed the median and the range of cumulative population-doubling (PD) levels. VEGF (20 ng/ml) significantly induced an increase of PD in HC-ECs, when compared untreated (UT) HC-ECs and the treatment with 1 μM of tofacitinib significantly decreased the effects of VEGF (**p = 0.007). (C) The histogram showed the median and the range of cumulative population-doubling (PD) levels. The PD of ECs treated with Tofacitinib 1 μM was comparable to PD of UT cells. D–F Representative image of immunofluorescence of ki67 expression (red) in HC-ECs cultured in untreated (UT) condition (D), treated with VEGF (E) and treated with VEGF+tofacitinib (F). Negative controls were obtained by omitting the primary antibody. Original magnification ×20. G The histogram showed the median and the range of the number of HC-ECs expressing ki67. VEGF significantly induced an increase of the number of HC-ECs ki67+, when compared to untreated (UT) HC-ECs and the treatment with tofacitinib significantly decreased the effects of VEGF (*p = 0.03; **p = 0.007)