Skip to main content
. 2015 Oct 23;124(7):957–965. doi: 10.1289/ehp.1509820

Figure 4.

Figure 4

Effects of developmental ­tetrachlorodibenzo-­p-dioxin (TCDD) exposure on bone marrow hematopoietic progenitor cells after ­long-­term competitive reconstitution. (A) ­c-­Kit versus Sca1 flow cytometry plots from the primary ­vehicle-­to-vehicle (V:V) competitive chimeras with CD45.1+lin cells in the left panel and CD45.2+lin cells in the right panel. The percentage of lin cells is specified by the number in each quadrant. (B) Flow cytometry plots from the primary vehicle to TCDD competitive chimeras. (C) Representative ­c-­Kit versus Sca1 flow cytometry plots from the ­vehicle-­to-vehicle secondary bone marrow chimera. (D) Flow cytometry plots from the secondary vehicle to TCDD (V:T) competitive chimeras. (E) Relative frequency of ­lin–­c-­Kit+Sca1+ (LSK) hematopoietic progenitor cells in the CD45.2 population of cells compared with the CD45.1 competitor cells from the primary and secondary chimeras. White bars compare ­vehicle-­to-vehicle chimeras, and blue bars compare the vehicle with TCDD chimeras. Solid bars are from the primary chimeras, and secondary chimeras are represented by bars containing slashes. The percentage of the control was calculated by dividing the frequency of ­c-­Kit+Sca1+ cells in the CD45.2+lin population by the same ­population of CD45.1+lin cells. Data are the mean ± SEM from n = 5 chimeras, and the experiment was repeated once. *** Denotes statistically significant by analysis of variance (ANOVA) followed by Tukey’s test; < 0.01 compared with the congenic cells from the same chimera.