Figure 3
Figure 3. Inhibition of TNF-α rescues erythroid defects in RPS19-deficient cord blood cells. Human CD34+ hematopoietic progenitor cells were infected with lentivirus carrying shRNA against RPS19 or Luc control, sorted for GFP+ cells after 72 hours, and treated with etanercept for 48 hours. (A) shRNA knockdown of RPS19 reduced RPS19 mRNA levels by approximately 70% compared with control. (B) Treatment of RPS19-deficient cord blood cells with etanercept reduced TNF-α and (C) p21 expression in these cells. (D) Etanercept treatment rescued both erythroid and myeloid colony formation of RPS19-deficient cells. Data are representative of 2 independent experiments. *P < .05; **P < .01; ***P < .001.

Inhibition of TNF-α rescues erythroid defects in RPS19-deficient cord blood cells. Human CD34+ hematopoietic progenitor cells were infected with lentivirus carrying shRNA against RPS19 or Luc control, sorted for GFP+ cells after 72 hours, and treated with etanercept for 48 hours. (A) shRNA knockdown of RPS19 reduced RPS19 mRNA levels by approximately 70% compared with control. (B) Treatment of RPS19-deficient cord blood cells with etanercept reduced TNF-α and (C) p21 expression in these cells. (D) Etanercept treatment rescued both erythroid and myeloid colony formation of RPS19-deficient cells. Data are representative of 2 independent experiments. *P < .05; **P < .01; ***P < .001.

Close Modal

or Create an Account

Close Modal
Close Modal