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. Author manuscript; available in PMC: 2017 Jul 1.
Published in final edited form as: J Allergy Clin Immunol. 2016 Mar 2;138(1):187–199. doi: 10.1016/j.jaci.2015.11.024

Figure 5. HUVECs permeability is regulated by STAT3-induced mir17–92 and can be restored in AD-HIES patient cells through the canonical Wnt signaling pathway.

Figure 5

(A) Western blot analysis of phosphorylated Src, total Src, and phosphorylated PTEN, in DMSO and C188–9 HUVECs following exposure to histamine (100 µM). (B–C) Western blot analysis of phosphorylated VE-cadherin, total VE-cadherin, active (non-phosphorylated) β-catenin, total β-catenin, phosphorylated Src, total Src, phosphorylated PTEN, total PTEN, and phosphorylated STAT3, in wild type and AD-HIES HUVECs following exposure to histamine (100 µM). Data are represented as the mean ± S.E.M. *p<0.05. (D) Real time PCR analysis of mir17–95 RNA expression in IL-11 (100ng/ml) treated wild type and AD-HIES HUVECs. Data are representative of 3 independent experiments. (E) Western analysis of SIAH1 and E2F1 expression in wild type and AD-HIES. Data are representative of 2 independent experiments. (F) Analysis of cytoplasmic verses nuclear active β-catenin in wild type and AD-HIES HUVECs.