Fig. 2: Manipulation of Clu levels in HSCs affects their differentiation.
From: Clusterin drives myeloid bias in aged hematopoietic stem cells by regulating mitochondrial function
a, Workflow for testing the role of Clu in regulating HSC lineage commitment in vivo. b,c, Frequency of lymphoid, myeloid, B, and T cells in mCherry+ peripheral blood cells at different time points after transplantation in recipient mice with Clu KO (b) or Clu OE (c) (n = 5 per group). d, FACS profile (left) and relative abundance of the HSPC populations (right) in the mCherry+ LSK (Lin− Sca1+ cKit+) derived from Clu KO oHSCs 4 months after transplantation in recipient mice compared with control mice (n = 3 per group). HSPC populations include LT-HSC (Cd150+ Cd48−), ST-HSC (Cd150− Cd48−), and MPP (Cd150− Cd48+). e, FACS profile (left) and relative abundance of the subpopulations (right) in the mCherry+ MPPs derived from Clu KO oHSCs 4 months after transplantation in recipient mice compared with control mice (n = 3 per group). MPP subpopulations include MPP3 (Cd135− Cd48+) and MPP4 (Cd135+ Cd48+). f, FACS profile (left) and relative abundance of the HSPC populations (right) in the mCherry+ LSK (Lin− Sca1+ cKit+) derived from Clu OE yHSCs 4 months after transplantation in recipient mice compared with control mice (n = 3 per group). g, FACS profile (left) and relative abundance of the subpopulations in the mCherry+ MPPs derived from Clu OE yHSCs 4 months after transplantation in recipient mice compared with control mice (n = 3 per group). Unpaired two-tailed Student’s t-test (b–g). Error bars represent mean ± standard deviation (s.d.) (b,c) or mean ± standard error of the mean (s.e.m.) (d–g). HSPC, hematopoietic stem and progenitor cell; ns, not significant; w, weeks.
