Fig. 1: Higher viability rates are found in splenic myeloid cells from SHP2D61Y mice compared to controls. | Cell Death & Disease

Fig. 1: Higher viability rates are found in splenic myeloid cells from SHP2D61Y mice compared to controls.

From: Oncogenic and microenvironmental signals drive cell type specific apoptosis resistance in juvenile myelomonocytic leukemia

Fig. 1

A Schematic representation of the experimental procedure. All experimental mice (controls -WT, MxCre, Ptpn11D61Y/+ and JMML mice - MxCre;Ptpn11D61Y/+) were injected with 300 μg poly I:C/mouse (in 3 doses every other day) to activate the oncogenic mutation. The experimental mice were analyzed at different stages of the disease: preleukemic - defined as stage 1 - S1 (5 weeks after polyI:C injection); leukemic - defined as stage 2 - S2 (5 months after polyI:C injection) and full-blown myeloproliferative disease - defined as stage 3 - S3 (7+ months after poly I:C injection - terminally ill mice). B Representative spleens are shown for: control mice (MxCre, Ptpn11D61Y/+) and JMML mice MxCre;Ptpn11D61Y/+ (S1, S2, S3). C Survival curves are shown for control mice (WT) and JMML MxCre;Ptpn11D61Y/+ mice. The percentage of live cells (AV 7AAD) was determined in the following splenic hematopoietic cell types: D CD11b+ myeloid cells; CD11b+Ly6Cmedium - circulatory monocytes; CD11b+Ly6Chigh - inflammatory monocytes and CD11b+Ly6G+ - neutrophils; E LSK - stem and progenitor hematopoietic cells, B220+ - B cells, TCR-β+ - T cells and Ter119+ - erythrocytes obtained from the spleen. All the above cell populations were determined ex vivo and assayed by flow cytometry for the indicated genotypes. The gating strategy was performed as described in Supplementary Fig. 7. All data are presented as mean ± SEM (n = 3–10; ≥5 independent experiments).

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