Differentiation Potential of Pancreatic Fibroblastoid Cells/Stellate Cells: Effects of Peroxisome Proliferator-Activated Receptor Gamma Ligands
Figure 3
Effects of PPARγ ligands on proliferation. (a) Time course of incubation of hPFC with 3.3 μM ciglitazone. Proliferation decreases significantly (*) over time. Reversibility was tested by washout of drug after 48 h and incubation in fresh drug-free medium for further 24 h, and the proliferation rate did not significantly differ from untreated cells. (b) Time course of incubation of PSC-1 cells with 3.3 μM ciglitazone. Proliferation rates decreased significantly (*) over time. The washout experiment did not show reversibility of ciglitazone-induced inhibition. (c) Effect of PPARγ ligands on PDGF-stimulated proliferation in hPFC. Cells were incubated for 24 h with platelet-derived growth factor (PDGF) at a concentration of 5 ng/mL. One hour after the start of PDGF incubation, ciglitazone (cig, 3.3 μM) or 15Δ-prostaglandin J2 (PGJ2, 5 μM) was added. PDGF induced a significant growth stimulation. Ciglitazone treatment did not significantly inhibit this growth induction, but PGJ2 did. (*Significant versus control, #significant versus PDGF stimulation.) (d) Effect of PPARγ ligands on PDGF-stimulated proliferation in HPF-T cells. Cells were incubated for 24 h with platelet-derived growth factor (PDGF) at a concentration of 5 ng/mL. One hour after start of PDGF incubation, ciglitazone (cig, 3.3 μM) or 15Δ-prostaglandin J2 (PGJ2, 5 μM) was added. PDGF stimulated proliferation significantly, and both ciglitazone and 15Δ-prostaglandin J2 inhibited stimulated growth in transformed HPF-T cells. (*Significant versus control, #significant versus PDGF stimulation, n ≥ 3.)
