Research Paper Volume 10, Issue 9 pp 2459—2479

MiR-665 aggravates heart failure via suppressing CD34-mediated coronary microvessel angiogenesis

Figure 3. MiR-665 directly targets CD34 by interaction with the 3′ UTR. (A) Real-Time PCR analysis of mRNA in association with Ago2 in HUVEC cells. Results from control were set to 1 (n=4). (B) Ago2 protein levels in co-immunoprecipitated products measured by Western blotting. (C) Representative immunohistochemical staining of CD34 in human heart (control, n = 2; heart failure [HF], n = 5). (D) Schematic representation of predicted target sites of miR-665 in the 3’ UTR of CD34. (E) Regulation of miR-665 on 3’ UTR of CD34 in HEK293 cell by luciferase reporter assay (n=4). (F) CD34 protein levels in treated HUVEC cells detected by Western blotting (n=4). (G) Stability curves of CD34 mRNA in treated HUVEC cells (n=3). Data are expressed as mean ± SEM.