PPAR-γ receptor ligands: novel therapy for pituitary adenomas
J. Clin. Invest. Anthony P. Heaney, et al. 111:1381 doi:10.1172/JCI16575 [Go to this article.]

Figure 2
PPAR-γ function in pituitary tumors. FACS and Western blot analysis of rosiglitazone-treated (10^–6 to 10^–5 M) human nonfunctioning and PRL-secreting pituitary tumor cells (a) and murine gonadotroph tumor cells (b) revealed increased number of cells in G₁ and decreased S phase (*P = 0.001; **P = 0.03) and a dose-dependent decrease in Ser⁷⁹⁵ phosphorylated retinoblastoma protein (c and d) in addition to decreased proliferating cell nuclear antigen (PCNA) and PRL expression (c). Northern blot analysis following rosiglitazone treatment revealed decreased expression of proliferative marker PTTG mRNA and PRL mRNA expression in rat GH3 cells (e) and decreased PTTG in αT3 gonadotroph cells (f). Rat testis RNA served as a positive control. 18S, β-actin markers, or Ponceau S staining confirmed RNA and protein loading. Ros, rosiglitazone; V, vehicle; M, RNAmarker.