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. 2013 Apr 24;123(5):2143–2154. doi: 10.1172/JCI64365

Figure 1. 16K PRL mediates antiangiogenic effects in ECs via miR-146a.

Figure 1

(A) miRNA level evaluated by qRT-PCR in HUVECs after 16K PRL treatment (50 nM, 8 hours). (B and C) miR-146a in HUVECs treated with 16K PRL (50 nM, 8 hours), (B) with or without BAY 11-7082 pretreatment (10 μM, 1 hour) or (C) with 72 hours transfection with p65 NF-κB subunit or control siRNA. (D) WT and mutated (Mut) miR-146a promoter luciferase vectors. (E) Luciferase activity after 16K PRL treatment (50 nM, 8 hours). (F) Proliferation status, reflected by BrdU incorporation, in HUVECs transfected with pre- or anti-miR-146a or -miR-control. (G) BrdU incorporation in HUVECs stimulated with 16K PRL (50 nM, 8 hours) with or without anti-miR-146a transfection (48 hours). (H) Apoptotic index, reflected by caspase-3 activity, in HUVECs transfected with pre- or anti-miR-146a or -miR-control. (I) Representative images of aortic rings 9 days after transfection with anti-miR-146a or -miR-control. Scale bars: 0.5 mm. (J) Quantification of sprout length in I (n = 8–10 aortic rings per condition). (K) Representative images of laser-induced choroidal neovascularization 7 days after transfection with pre-miR-control and -miR-146a injected intravitreously (n ≥ 8 eyes/condition; 4 lesions/eyes). Dashed outlines denote lesion area. Scale bars: 100 μm. (L) Quantification of the green signal present in lesion area. Data are mean ± SD (n ≥ 3) or mean ± SEM (J and L). *P < 0.05 vs. respective control. #P < 0.05 vs. 16K PRL–treated control. See also Supplemental Figure 1.