Figure 1
Figure 1. Overexpression of miR-17-92 in mice leads to expansion of multipotent hematopoietic progenitor cells. (A) A representative photograph (top panel) and average spleen weights of empty vector control vector (n = 6) and miR-17-92 mice (n = 8), 16 weeks after infection (bottom panel), where error bars represent SD; **P < .005. (B) H&E stained paraffin sections of spleens from empty vector control and miR-17-92 mice 16 weeks after infection (scale bar, 1 mm). Data are representative sections from 3 staining experiments. (C) Quantitative RT-PCR analysis of precursor miR-17-92 expression in the spleens isolated from empty vector control (n = 4) and miR-17-92 mice (n = 4) 16 weeks after infection. Results were normalized relative to β-actin expression in all experimental samples. Each experiment was performed in quadruplicate, where error bars represent SD; ***P < .0005. (D) Frequency of hematopoietic cell surface marker expression, as a percentage of total splenocytes (top panel) and bone marrow cells (bottom panel) isolated from uninfected (n = 3), empty vector control (n = 4), and miR-17-92 mice (n = 4). Values represent the mean % ± SD; *P < .05 (E) in vitro colony assays displaying the kinetics of CFU colony expansion of miR-17-92 or empty vector control injected mice (n = 6) splenocytes (top panel) and BM cells (bottom panel). Three CFU types were scored: CFU-GM, BFU-E, and CFU-GEMM. Colony counts were performed in triplicate after 5 to 14 days of culture, where error bars represent SD; *P < .05, **P < .005, and ***P < .0005.

Overexpression of miR-17-92 in mice leads to expansion of multipotent hematopoietic progenitor cells. (A) A representative photograph (top panel) and average spleen weights of empty vector control vector (n = 6) and miR-17-92 mice (n = 8), 16 weeks after infection (bottom panel), where error bars represent SD; **P < .005. (B) H&E stained paraffin sections of spleens from empty vector control and miR-17-92 mice 16 weeks after infection (scale bar, 1 mm). Data are representative sections from 3 staining experiments. (C) Quantitative RT-PCR analysis of precursor miR-17-92 expression in the spleens isolated from empty vector control (n = 4) and miR-17-92 mice (n = 4) 16 weeks after infection. Results were normalized relative to β-actin expression in all experimental samples. Each experiment was performed in quadruplicate, where error bars represent SD; ***P < .0005. (D) Frequency of hematopoietic cell surface marker expression, as a percentage of total splenocytes (top panel) and bone marrow cells (bottom panel) isolated from uninfected (n = 3), empty vector control (n = 4), and miR-17-92 mice (n = 4). Values represent the mean % ± SD; *P < .05 (E) in vitro colony assays displaying the kinetics of CFU colony expansion of miR-17-92 or empty vector control injected mice (n = 6) splenocytes (top panel) and BM cells (bottom panel). Three CFU types were scored: CFU-GM, BFU-E, and CFU-GEMM. Colony counts were performed in triplicate after 5 to 14 days of culture, where error bars represent SD; *P < .05, **P < .005, and ***P < .0005.

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