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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 8. — AMP-activated protein kinase (AMPK) regulates levels of isocitrate dehydrogenases and α-ketoglutarate. Neutrophils from wild-type (WT) and AMPKα2^ΔMC (ΔMC) littermates were incubated under normoxic (Nox) or hypoxic (Hox) conditions for 16 h (n=6 per group). A, Isocitrate dehydrogenase (IDH) 1 and IDH3b expression (label-free quantification intensity). B, Western blot confirmation of altered IDH1 and IDH3b expression. C, α-Ketoglutarate (α-KG) levels in neutrophils from WT and ΔMC littermates incubated under Nox or Hox conditions for 16 h (n=5–6 per group). D, HIF-1α levels in THP-1 cells incubated in Hox conditions for 6 h with indicated concentrations of octyl-α-KG, a cell-permeable ester of α-KG (n=6 independent experiments). *P<0.05, **P<0.01, ***P<0.001.