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. 2011 May 2;121(6):2361–2370. doi: 10.1172/JCI45213

Figure 4. Alteration of the TGF-β pathway in aging Tif1gΔ/Δ mice.

Figure 4

(A) Defective TGF-β signaling pathway responsiveness in Tif1gΔ/Δ mice. Sorted ST-HSCs/MPPs were plated on methylcellulose medium in triplicate, with or without TGF-β and TGF-β inhibitor (inh.). The number of myeloid colonies was determined at day 8. The results are shown as the mean ± SD of triplicates. (B) Representative images (original magnification, ×138) of the resulting myeloid colonies from sorted ST-HSCs/MPPs, untreated or treated with TGF-β or with TGF-β plus TGF-β inhibitor. (C and D) TGF-β–neutralizing antibody (αTGF-β) does not affect hematopoietic progenitor cell distribution in Tif1gΔ/Δ mice. (C) Analysis of LSK cells from treated or untreated representative control and Tif1gΔ/Δ mice demonstrated an increase in the LSK population in control mice treated with the antibody, which was not observed in Tif1gΔ/Δ mice. (D) Analysis of ST-HSCs/ MPPs from treated or untreated representative control and Tif1gΔ/Δ mice demonstrated an increase in MPPs in control mice treated with the antibody, which was not observed in Tif1gΔ/Δ mice.