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. 2017 Oct 19;6(10):e006680. doi: 10.1161/JAHA.117.006680

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© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.

This is an open access article under the terms of the Creative Commons Attribution‐NonCommercial‐NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made.

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PHD3 overexpression mitigates IH‐induced HIF‐1α activation in endothelial cells. A, Western blot analysis and quantification of HIF‐1α (a1 and a2), PHD3 (a1 and a3). B, Representative images of immunofluorescence staining with antibodies to HIF‐1α (red). Nuclei were counterstained with DAPI (blue; original magnification, ×400; bars=20 μm). *P<0.05 vs control; ^# P<0.05 vs IH+LvNC; ^## P<0.01 vs IH+LvNC; ^& P<0.05 vs IH+shNC. DAPI indicates 4',6‐diamidino‐2‐phenylindole; HIF‐1, hypoxia‐inducible factor 1 alpha; IH, intermittent hypoxia; LvPHD3, lentivirus carrying PHD3 cDNA; PHD3, prolyl 4‐hydroxylase domain protein 3; shPHD3, short‐hairpin PHD3.