FGFR1 inactivation impairs megakaryocyte proliferation and FGF production induced by BM damage. (A) Cytospin followed by H&E staining and comparison of the frequency and absolute number of FSC^hi CD41-positive population in BM cells pre and post–2-week culture (n = 3). (B) Flow cytometric analyses of BM FSC^hiCD41⁺ cells and gene expression analysis of Fgfr1 using qRT-PCR on BM FSC^hiCD41⁺ and non-FSC^hiCD41⁺ cells from C57Bl/6 WT mice on the days indicated after 5FU (n = 4). (C) Mks stained using VWF (red) and hematoxylin (blue) to label nuclei. Quantification of the numbers of VWF⁺ Mks per field of view from BM and representative BM sections of Fgfr1 Mx1:Control, Mx1:CKO mice at 10 days after 5FU compared with day 0 (n = 3). (D) Quantification of CFU-Mks and representative CFU-Mk (brown colonies) from Fgfr1 Scl:Control, Scl:CKO BM at 12 days after 5FU. Representative data from 2 independent experiments. (E) Mks attached to blood vessel stained by VWF at 10 days after 5FU. (F) Gene expression analysis of Fgf1, 2 and 10 using qRT-PCR on BM Mks (FSC^hiCD41⁺ cells) from Fgfr1 Scl:Control and Scl:CKO mice on the days indicated after 5FU. (G-H) Expression analysis of FGFR1(G) and FGF1(H) using mean fluorescence intensity (MFI) on BM Mks (FSC^hiCD41⁺ cells) from FVB/N WT and FVB/N Fgf2 KO mice (n = 4).