Vascular Endothelial Growth Factors C and D Induces Proliferation of Lymphangioleiomyomatosis Cells through Autocrine Crosstalk with Endothelium
Am J Pathol Issaka et al. 175: 1410
Supplemental Material
This supplemental material includes supporting data for this study.
Files in this Data Supplement:
- Supplemental Figure 1 - (A) Proliferation of LDC, measured as the extent of BrdU uptake, in LDC grown on varying concentrations of VEGF-C in the absence (diamonds) or presence of 10 µM MAZ-51 (R3 inhibitor, squares) or the PI3K inhibitor, 3 nM wortmannin (triangles). (B) Western blots to detect phospho-ErkMAP kinase (pErk) in lysates from untransfected LDC (left panel) or LDC expressing GFP tagged wtTSC2 (right panel) in response to VEGF-R3 specific agonist VEGF-C (Cys156Ser) in the absence or presence of the VEGF-R3 inhibitor, MAZ-51, over time; total Erk-2 serves as a protein loading control. (C) Photomicrograph to demonstrate high efficiency of gene delivery into LDC.
