American Society of Hematology

Figure 4

$Figure 4. Molecular myeloid priming exists in fractionated LT-HSCs from arthritic mice. (A) Quantification of Ki67-negative (quiescent) fraction of HSCs. (B) Quantitative real-time PCR of myeloid inflammatory signature genes (see Figure 3B,D) in arthritic and control HSCs (CD150+CD48−CD34−KSL IL7Rα−). (C) Table comparing fold increase in expression of myeloid inflammatory signature genes in arthritic KSL cells and HSCs relative to controls (based on Figures 3B,D, 4B); *P < .05, **P < .01 relative to control KSL or control KSL-derived cells (see also supplemental Figure 6).$

Molecular myeloid priming exists in fractionated LT-HSCs from arthritic mice. (A) Quantification of Ki67-negative (quiescent) fraction of HSCs. (B) Quantitative real-time PCR of myeloid inflammatory signature genes (see Figure 3B,D) in arthritic and control HSCs (CD150⁺CD48⁻CD34⁻KSL IL7Rα⁻). (C) Table comparing fold increase in expression of myeloid inflammatory signature genes in arthritic KSL cells and HSCs relative to controls (based on Figures 3B,D, 4B); *P < .05, **P < .01 relative to control KSL or control KSL-derived cells (see also supplemental Figure 6).

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