Role of PPARγ. (A) Transcriptional activity of a PPAR-driven reporter gene in COS-7 cells cotransfected with PPARγ/RXRα and with Prdm16(B6) or Prdm16(D2) expression vectors in the presence or absence of rosiglitazone (1μM) (luciferase values relative to renilla luciferase activity; n = 9). (B) Effect of rosiglitazone (1μM) on FLT3L (left) or KL/TPO (middle) supported proliferation of LSK cells from C57BL/6 mice (n = 4; *P < .05), and on FLT3L-supported proliferation of B6.D2-chr.4 congenic mice (right; 1 triplicate experiment). Data were normalized across experiments to proliferation observed at 10 ng/mL FLT3L and DMSO control. (C) Effect of rosiglitazone on FLT3L-induced and KL/TPO-induced proliferation of C57BL/6 LSK cells in the presence and absence of SB431542 (n = 3 triplicate experiments; data expressed as percentage of the proliferation at 10 ng/mL of each cytokine). (D) Effect of GW9662 (1μM) on FLT3L (left) and KL/TPO (right) supported proliferation of C57BL/6 LSK cells in serum-containing cultures (n ≥ 4; *P = .03; data expressed as percentage of the proliferation at 10 ng/mL of each cytokine.). (E) FLT3L- and KL/TPO-supported proliferation of LSK cells isolated from mice fed with chow or rosiglitazone for 3 weeks in the presence of 10% serum (*P < .05; n = 6). (F) PB white blood cell (WBC) counts in FLT3^−/− and wt mice gavaged with rosiglitazone (15 mg/kg) or DMSO daily on days 0-4 after administration of 5-FU on day 0 (150 mg/kg intraperitoneally; n = 10; *P < .05 compared with wt DMSO).