title: Rosiglitazone, PPAR-gamma receptor ligand, decreases the viability of rat prolactin-secreting pituitary tumor cells in vitro.
abstract: OBJECTIVE
  PPAR-gamma is a member of the nuclear receptor superfamily. PPAR-gamma activation is associated with glucose metabolism regulation, adipocyte differentiation, inhibition of macrophage and monocyte activation and anti-angiogenesis. PPAR-gamma ligands thiazolidinediones (TZDs) have been shown to inhibit the growth and secretory activity of several rat and murine pituitary tumors in vivo as well as in vitro (ACTH-secreting AtT20, PRL- and GH-secreting GH3, LH-secreting LbetaT2 and alpha-T3 cells). TZDs have been demonstrated to induce G0-G1 cell-cycle arrest and apoptosis in human, rat somatolactotroph, murine corticotroph and gonadotroph pituitary tumor cells. In the present study we have investigated for the first time the effects of PPAR-gamma receptor ligand rosiglitazone on the rat estrogens-induced, PRL-secreting pituitary tumor cells in vitro.
  
  
  METHODS
  Four weeks old male Fischer 344 rats were used in the experiment. Pituitary tumors were induced by subcutaneous implantation of capsules containing diethylstilboestrol (DES). Eight weeks after the implantation of capsules the rats were sacrificed and pituitary tumors were collected. Tumorous cells were isolated and exposed in the primary culture to rosiglitazone at the concentrations 10(-10) - 10(-4)M for 24 hours. The cell growth was estimated by the measurement of the cells metabolic activity using the EZ4U system.
  
  
  RESULTS
  We have demonstrated that rosiglitazone at the concentrations 10(-10) - 10(-4)M significantly decreases the number of viable rat PRL-secreting pituitary tumor cells in vitro.
  
  
  CONCLUSIONS
  These results suggest that PPAR-gamma receptor agonists thiazolidinediones may be useful in the medical treatment of pituitary tumors.
authors.affiliation: Institute of Endocrinology, Medical University of Lodz, Poland. gruszka.a@op.pl
authors.forename: Anna
authors.initials: A
authors.lastname: Gruszka
authors.forename: Jolanta
authors.initials: J
authors.lastname: Kunert-Radek
authors.forename: Marek
authors.initials: M
authors.lastname: Pawlikowski
mesh_terms: D000818:Animals; D002273:Carcinogens / Q000008:administration & dosage / Q000494:pharmacology; D002470:Cell Survival / Q000187:drug effects; D004054:Diethylstilbestrol / Q000008:administration & dosage / Q000494:pharmacology; D004343:Drug Implants; D007004:Hypoglycemic Agents / Q000494:pharmacology*; D008024:Ligands; D008297:Male; D047495:PPAR gamma / Q000187:drug effects*; D010911:Pituitary Neoplasms / Q000139:chemically induced / Q000378:metabolism*; D011388:Prolactin / Q000378:metabolism*; D051381:Rats; D011916:Rats, Inbred F344; D000077154:Rosiglitazone; D045162:Thiazolidinediones / Q000494:pharmacology*; D014407:Tumor Cells, Cultured
chemical_list: D002273:Carcinogens; D004343:Drug Implants; D007004:Hypoglycemic Agents; D008024:Ligands; D047495:PPAR gamma; D045162:Thiazolidinediones; D000077154:Rosiglitazone; D004054:Diethylstilbestrol; D011388:Prolactin