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. Author manuscript; available in PMC: 2015 Dec 16.
Published in final edited form as: J Am Coll Cardiol. 2015 Jun 16;65(23):2526–2537. doi: 10.1016/j.jacc.2015.03.570

FIGURE 5. IGF-1R/PI3K-Akt: Downstream Signaling Pathway of miR-223 in VSMCs.

FIGURE 5

(A) Computational analysis suggests that human insulin-like growth factor 1 receptor (IGF-1R) has an miR-223 binding site in its 3′-UTR. (B) Representative Western blots show IGF-1R protein levels from different groups. Overexpression of miR-223 decreased the expression of IGF-1R at (C) the protein level and the (D) messenger RNA (mRNA) level in VSMCs. (E) Luciferase assay in HEK 293 cells co-transfected with a fragment of the 3′-UTR of IGF-1R mRNA containing the conserved miR-223 binding sequence, and either vehicle, an empty plasmid (pDNR-CMV), or a plasmid expressing miR-223 (pmiR-223). An IGF-1R 3′-UTR mutated fragment was used as a mutated control group. (F) Representative Western blots show IGF-1R protein levels in aortas from miR-223 knockout mice and wild-type control mice. (G) IGF-1R expression in aortas from miR-223 knockout mice was higher than that from wild-type control mice. (H) Representative Western blots show p-AKT and total AKT (t-AKT) from different groups. (I) Overexpression of miR-223 decreased expression of p-AKT in VSMCs. *p < 0.05 compared with control groups. GADPH = glyceraldehyde-3-phosphate dehydrogenase; hsa = human; other abbreviations as in Figure 1.