American Society of Hematology

Figure 3

$Figure 3. Kinetin riboside targets phenotypic CD34+CD38− L-ICs. KR induced apoptosis (annexin-V+) in phenotypic CD34+CD38− L-ICs, but not CD34+CD38− HSCs after overnight treatment. Eleven primary AML samples (A-C) or 9-12 separate pools of Lin− CB cells (D-F) were cultured for 16 hours with DMSO vehicle (black), 10μM KR (white), or 5μM PTL (gray). The frequency of apoptotic cells in CD34+ (A,D) and CD34+CD38− (B,E) fractions. (C) PTL reduced the frequency of CD14+ AML cells. (F) KR or PTL did not reduce the frequency of phenotypic Lin− CB HSC (CD34+CD38−). (G-H) Progenitor cell activity was measured by plating 3 separate pools of Lin− CB cells in methylcellulose in the presence of KR or PTL and counting myeloid (G) or erythroid (H) colonies (*P < .05, **P < .01, and ***P < .001).$

Kinetin riboside targets phenotypic CD34⁺CD38⁻ L-ICs. KR induced apoptosis (annexin-V⁺) in phenotypic CD34⁺CD38⁻ L-ICs, but not CD34⁺CD38⁻ HSCs after overnight treatment. Eleven primary AML samples (A-C) or 9-12 separate pools of Lin⁻ CB cells (D-F) were cultured for 16 hours with DMSO vehicle (black), 10μM KR (white), or 5μM PTL (gray). The frequency of apoptotic cells in CD34⁺ (A,D) and CD34⁺CD38⁻ (B,E) fractions. (C) PTL reduced the frequency of CD14⁺ AML cells. (F) KR or PTL did not reduce the frequency of phenotypic Lin⁻ CB HSC (CD34⁺CD38⁻). (G-H) Progenitor cell activity was measured by plating 3 separate pools of Lin⁻ CB cells in methylcellulose in the presence of KR or PTL and counting myeloid (G) or erythroid (H) colonies (*P < .05, **P < .01, and ***P < .001).

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