Figure 6.
Figure 6. Atorvastatin and NAC improved megakaryocytopoiesis in BM CD34+ cells cocultured with BM EPCs from corticosteroid-resistant ITP patients. Even though the (A) percentages of BM CD34+ cells among corticosteroid-resistant ITP, corticosteroid-sensitive ITP, and healthy controls showed no significant differences, the (B) intracellular ROS levels and (C) apoptosis rates of BM CD34+ cells were increased in the corticosteroid-resistant ITP group. (D) The CFU-plating efficiency of BM CD34+ cells from corticosteroid-resistant ITP, corticosteroid-sensitive ITP, and healthy controls was analyzed. The megakaryocyte production, maturation, platelet release, and CFU-MK–plating efficiencies in BM CD34+ cells were analyzed after coculture with the differently treated BM EPCs from corticosteroid-resistant ITP. The (E) percentages of megakaryocytes, (F) megakaryocyte apoptosis, (G) megakaryocyte ploidy distribution, (H) platelet release, and (I-J) CFU-MK counts were analyzed after 12 days of coculture. CFU-MKs were stained with mouse anti–human GPIIb/IIIa antibody and biotin-conjugated goat anti–mouse IgG, then counterstained with Evans Blue. CFU-MK colonies were defined as groups of 3 or more GPIIb/IIIa-positive cells (pink membranes with blue nuclei) (scale bars, 200 μm). The data were expressed as fold change relative to corticosteroid-resistant ITP. Subject variables were compared using the Mann-Whitney U test for continuous variables. All P values <.05 were considered significant and were provided in the figure. ST, atorvastatin.

Atorvastatin and NAC improved megakaryocytopoiesis in BM CD34+cells cocultured with BM EPCs from corticosteroid-resistant ITP patients. Even though the (A) percentages of BM CD34+ cells among corticosteroid-resistant ITP, corticosteroid-sensitive ITP, and healthy controls showed no significant differences, the (B) intracellular ROS levels and (C) apoptosis rates of BM CD34+ cells were increased in the corticosteroid-resistant ITP group. (D) The CFU-plating efficiency of BM CD34+ cells from corticosteroid-resistant ITP, corticosteroid-sensitive ITP, and healthy controls was analyzed. The megakaryocyte production, maturation, platelet release, and CFU-MK–plating efficiencies in BM CD34+ cells were analyzed after coculture with the differently treated BM EPCs from corticosteroid-resistant ITP. The (E) percentages of megakaryocytes, (F) megakaryocyte apoptosis, (G) megakaryocyte ploidy distribution, (H) platelet release, and (I-J) CFU-MK counts were analyzed after 12 days of coculture. CFU-MKs were stained with mouse anti–human GPIIb/IIIa antibody and biotin-conjugated goat anti–mouse IgG, then counterstained with Evans Blue. CFU-MK colonies were defined as groups of 3 or more GPIIb/IIIa-positive cells (pink membranes with blue nuclei) (scale bars, 200 μm). The data were expressed as fold change relative to corticosteroid-resistant ITP. Subject variables were compared using the Mann-Whitney U test for continuous variables. All P values <.05 were considered significant and were provided in the figure. ST, atorvastatin.

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