Fig 2: The effect of nerve growth factor (NGF) in epithelial cells permeabilized apically with nystatin. Cells were placed into Ussing chambers and allowed to equilibrate prior to adding nystatin (50 µmol/L) to the apical chamber. Nystatin caused a large increase in Isc. Responses to ouabain were generated in the (A) absence (vehicle control – modified Krebs-Henseleit solution [MKHS]) or (B) presence of 1 ng/mL NGF. NGF did not elicit bioelectric responses when applied apically to the permeabilized cells, and did not alter Na+/K+-ATPase activity as there were no differences in the response to ouabain. Control n = 6, NGF n = 4. Scale bar = 10 min.

Fig 3: Effect of nerve growth factor (NGF) on ion transport. Responses to (A) amiloride, (B) NPPB, and (C) ouabain were calculated as a percent change from baseline (4 donors). NGF significantly reduced the amiloride response (P = 0.0127).

Fig 4: Immunohistochemical localization of NGF in breast tumors. A, CA breast (IDC), intense NGF expression in ductal epithelium (black arrows) and small vessels (green arrows), Ad—adipocyte. B, Phyllodes tumor, intense expression in ductal epithelium (black arrows) and stroma (green arrows). C, Fibroadenoma, negligible expression, tissue counterstained with hematoxylin (H) to show nuclei of fibrocytes, characteristic of fibroadenoma (black arrows). (Scale bar, resolution 200 µm, is marked by bracket at the upper left corner of images)

Fig 5: Characteristics of hADSC. (A) Capacity of differentiation of hADSCs. The cells were stained by Oil red O (adipogenic differentiation), Alizarin Red S (osteogenic differentiation), and Safranin O (chondrogenic differentiation). (B) Immunophenotype of hADSCs was carried out using flow cytometry for the following markers: SSEA-4, CD34, CD90, CD105, and HLA-DR. Karyotype of hADSC (C) and the concentration of NGF and BDNF released by hADSCs (D). F.M.; fresh medium, C.M.; conditioned medium, n.d.; not detected.