Figure 2
Figure 2. Stiffness of leukemic cells increases with progression of cell death and is attenuated by disruption of the actin cytoskeleton. (A) A typical stiffness trace of a single M5 AML cell exposed to 1 μM daunorubicin (red circles). The apparent stiffness of a typical control cell remains relatively constant (green triangles) and does not undergo apoptosis or cell death during the course of the experiment. Error bars represent standard error. (B) From the same patient sample, the average apparent stiffness of a population of late apoptotic/dead AML cells was significantly stiffer than early apoptotic cells and controls (n = 15, P < .05). (C) Cell stiffness increases faster with 1 μM daunorubicin (DNR, in red) than 1 μM dexamethasone (DEX, in green). Solid and dotted lines represent myeloid and lymphoid leukemia cells, respectively. Transition from open to filled shapes represent onset of cell death (PI-positive staining). (D) Exposure to 2 μM cytochalasin D, an actin polymerization inhibitor, reduces stiffening behavior in HL60 cells exposed to 1 μM daunorubicin. The cells represented by these 3 lines were exposed to daunorubicin at time 0 minutes. The cell represented by the green line was also exposed to cytochalasin D at time 0 minutes (vertical green dashed line) and exhibited little stiffening behavior. The cell represented by the blue line was exposed to cytochalasin D after 45 minutes (vertical blue dashed line) and exhibited little stiffening behavior after exposure. As a positive control, the cell represented by the red line was not exposed to cytochalasin D. (E) HL60 and Jurkat cells were incubated with 1 μM daunorubicin and 2 μM cytochalasin D. The average stiffness of dead HL60 cells (n = 15) exposed to daunorubicin and cytochalasin D (green) was 0.2 kPa ± 0.05 kPa, whereas the average stiffness of dead HL60 cells exposed to daunorubicin alone (red) was 1.2 kPa ± 0.3 kPa (P < .05). Likewise, the average stiffness of dead Jurkat cells (n = 15) exposed to daunorubicin and cytochalasin D (green) was 0.1 kPa ± 0.03 kPa, whereas the average stiffness of dead Jurkat cells exposed to daunorubicin alone (red) was 0.5 kPa ± 0.14 kPa (P < .05).

Stiffness of leukemic cells increases with progression of cell death and is attenuated by disruption of the actin cytoskeleton. (A) A typical stiffness trace of a single M5 AML cell exposed to 1 μM daunorubicin (red circles). The apparent stiffness of a typical control cell remains relatively constant (green triangles) and does not undergo apoptosis or cell death during the course of the experiment. Error bars represent standard error. (B) From the same patient sample, the average apparent stiffness of a population of late apoptotic/dead AML cells was significantly stiffer than early apoptotic cells and controls (n = 15, P < .05). (C) Cell stiffness increases faster with 1 μM daunorubicin (DNR, in red) than 1 μM dexamethasone (DEX, in green). Solid and dotted lines represent myeloid and lymphoid leukemia cells, respectively. Transition from open to filled shapes represent onset of cell death (PI-positive staining). (D) Exposure to 2 μM cytochalasin D, an actin polymerization inhibitor, reduces stiffening behavior in HL60 cells exposed to 1 μM daunorubicin. The cells represented by these 3 lines were exposed to daunorubicin at time 0 minutes. The cell represented by the green line was also exposed to cytochalasin D at time 0 minutes (vertical green dashed line) and exhibited little stiffening behavior. The cell represented by the blue line was exposed to cytochalasin D after 45 minutes (vertical blue dashed line) and exhibited little stiffening behavior after exposure. As a positive control, the cell represented by the red line was not exposed to cytochalasin D. (E) HL60 and Jurkat cells were incubated with 1 μM daunorubicin and 2 μM cytochalasin D. The average stiffness of dead HL60 cells (n = 15) exposed to daunorubicin and cytochalasin D (green) was 0.2 kPa ± 0.05 kPa, whereas the average stiffness of dead HL60 cells exposed to daunorubicin alone (red) was 1.2 kPa ± 0.3 kPa (P < .05). Likewise, the average stiffness of dead Jurkat cells (n = 15) exposed to daunorubicin and cytochalasin D (green) was 0.1 kPa ± 0.03 kPa, whereas the average stiffness of dead Jurkat cells exposed to daunorubicin alone (red) was 0.5 kPa ± 0.14 kPa (P < .05).

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