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. 2017 Jan 5;120(1):99–109. doi: 10.1161/CIRCRESAHA.116.309937

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© 2016 The Authors.

Circulation Research is published on behalf of the American Heart Association, Inc., by Wolters Kluwer Health, Inc. This is an open access article under the terms of the Creative Commons Attribution Non-Commercial-NoDervis License, which permits use, distribution, and reproduction in any medium, provided that the original work is properly cited, the use is noncommercial, and no modifications or adaptations are made.

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Figure 6. — Link between AMP-activated protein kinase (AMPK) α2 and hypoxia-inducible factor-1α (HIF-1α). A, Pie charts depicting significantly regulated proteins in neutrophils from wild-type (WT) and AMPKα2^ΔMC (ΔMC) mice after 16-h exposure to hypoxia. Upper: total number of significantly regulated proteins. Lower: number of significantly up- and downregulated proteins. B, HIF-1α levels in HEK293 cells transfected with a control siRNA (CTL) or siRNA directed against AMPKα1 (siα1) or AMPKα2 (siα2) and then either maintained under normoxic conditions, exposed to hypoxia (1% O₂, 6 h) or stimulated with CoCl₂ (150 µmol/L, 6 h). Graphs summarize data from 5 independent experiments. C, HEK293 cells transfected with a control siRNA (siCTL) or siRNA-directed against AMPKα2 (siα2) were exposed to hypoxia in the presence of solvent (Solv) or dimethyloxalylglycine (DMOG; 1 mmol/L) for 16 h. HIF-1α levels and its hydroxylation on proline 564 (OH-P564) were analyzed by Western blotting (n=9–12 per group). The break in the blots indicates that nonadjacent lanes in the same Western blot are presented. *P<0.05, **P<0.01, ***P<0.001.