Figure 5
Figure 5. Treatment with mir21 inhibitor leads to an increase in red blood cells in TGF-β transgenic mice. (A) Mice expressing TGF-β (Alb/TGFβ+) were treated with LNA-modified anti–miR-21 (n = 7) or mismatched placebo controls (n = 6) for 5 doses. Mice treated with anti–miR-21 oligos had a significant increase in hematocrit (HCT, Student’s t-test, P = .03), hemoglobin (Hgb [gm/DL], Student’s t-test, P = .049), and red blood cells (RBCs [×106], Student’s t-test, P = .0005). (B) Equal numbers of bone marrow cells were grown in methylcellulose and demonstrated increased erythroid colony formation in the mice treated with miR-21 inhibitor (n = 5 in each group, Student’s t-test, P = .04. (C) Representative bone marrow biopsy samples from both groups show an increase in SMAD7 levels in the treatment group with a corresponding decrease in phospho-SMAD2.

Treatment with mir21 inhibitor leads to an increase in red blood cells in TGF-β transgenic mice. (A) Mice expressing TGF-β (Alb/TGFβ+) were treated with LNA-modified anti–miR-21 (n = 7) or mismatched placebo controls (n = 6) for 5 doses. Mice treated with anti–miR-21 oligos had a significant increase in hematocrit (HCT, Student’s t-test, P = .03), hemoglobin (Hgb [gm/DL], Student’s t-test, P = .049), and red blood cells (RBCs [×106], Student’s t-test, P = .0005). (B) Equal numbers of bone marrow cells were grown in methylcellulose and demonstrated increased erythroid colony formation in the mice treated with miR-21 inhibitor (n = 5 in each group, Student’s t-test, P = .04. (C) Representative bone marrow biopsy samples from both groups show an increase in SMAD7 levels in the treatment group with a corresponding decrease in phospho-SMAD2.

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