Figure 1.
Figure 1. Macrophage differentiation by estradiol-inducible IRF-8/ER chimera in Irf-8-/- myeloid progenitor cells. (A) Diagram of the IRF-8/hormone-binding domain of the estrogen receptor (IRF-8/ER). (B) Wright-Giemsa–stained Irf-8-/- myeloid progenitor Tot2 cells transduced with a retrovirus carrying ER or IRF-8/ER (original magnification, × 1000). Cells were either left untreated or treated with 1 μM β-estradiol (Est) for 24 hours. (C) Semiquantitative RT-PCR analysis for macrophage differentiation-related genes. RNA from cells treated with 1 μM β-estradiol for the indicated time was subjected to semiquantitative RT-PCR for c-fms and scavenger receptor (SR) expression. Cells treated with 1 μM β-estradiol for 3 days were also analyzed for expression of IL-12p40, inducible nitric oxide synthase (iNOS), and Fcγ receptor I (FcγRI) transcripts. β-actin was used as the loading control.

Macrophage differentiation by estradiol-inducible IRF-8/ER chimera in Irf-8-/- myeloid progenitor cells. (A) Diagram of the IRF-8/hormone-binding domain of the estrogen receptor (IRF-8/ER). (B) Wright-Giemsa–stained Irf-8-/- myeloid progenitor Tot2 cells transduced with a retrovirus carrying ER or IRF-8/ER (original magnification, × 1000). Cells were either left untreated or treated with 1 μM β-estradiol (Est) for 24 hours. (C) Semiquantitative RT-PCR analysis for macrophage differentiation-related genes. RNA from cells treated with 1 μM β-estradiol for the indicated time was subjected to semiquantitative RT-PCR for c-fms and scavenger receptor (SR) expression. Cells treated with 1 μM β-estradiol for 3 days were also analyzed for expression of IL-12p40, inducible nitric oxide synthase (iNOS), and Fcγ receptor I (FcγRI) transcripts. β-actin was used as the loading control.

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