Fig 1: VEPTP inhibition with an extracellular domain targeting antibody mAb 109.1 induces Tie2 and ERK1/2 phosphorylation and protects against VEGF‐A induced vascular permeability in mouse endothelial cells. (a) Mouse endothelial cells (bEnd.3, ATCC) were treated with increasing concentrations of mAb 109.1 (purple circles) or the isotype (black circles). mAb 109.1 treatment resulted in a dose dependent increase in phospho‐Tie2:total Tie2 ratio. (b) mAb 109.1 treatment (purple circles) resulted in a dose‐dependent increase in the phospho‐ERK1/2:ERK1/2 ratio. (c) VEGF‐A (500 ng/mL) treatment significantly increased permeability of FITC‐dextran across confluent mouse endothelial monolayer on transwell membranes. VEGF‐A induced endothelial monolayer permeability was significantly blocked by mAb 109.1 treatment at both 50 and 100 nM concentrations. (d, e) qPCR analyses showed that mAb 109.1 treatment (at 50 and 100 nM) of mouse endothelial cells resulted in a significant decrease in Angpt2 and Edn1 expression. VEPTP, vascular endothelial protein tyrosine phosphatase; Tie2, tyrosine kinase with immunoglobulin and epidermal growth factor homology domains 2; ERK1/2, extracellular signal‐regulated kinase 1/2; VEGF‐A, vascular endothelial growth factor A; FITC‐dextran, fluorescein isothiocyanate dextran; qPCR, quantitative polymerase chain reaction; Angpt2, angiopoietin‐2; Edn1, endothelin‐1; Ppia, Peptidylprolyl isomerase A.