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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 5. — Effect of AMP-activated protein kinase (AMPK) α2 deletion on neutrophil apoptosis. 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, Translocase of inner mitochondrial membrane 50 (TIM50) label-free quantification (LFQ) intensity (left) and Western blot of neutrophils maintained under hypoxic conditions (right). B, Api5 LFQ intensity (left) and Western blot of neutrophils maintained under hypoxic conditions (right). C, Expression of cleaved caspase-3 (Cl. Casp. 3) and Bax in bone marrow–derived neutrophils from wild-type (WT) and AMPKα2^ΔMC (ΔMC) littermates (n=8 per group for Cl. Casp. 3 and n=5 per group for Bax expression). D, Caspase-3/7 activity measured as DEVD (7-amino-4-trifluoromethyl coumarin) fluorescence after cleavage from Asp-Glu-Val-Asp in neutrophils from WT and ΔMC littermates (n=5 per group). Cells were incubated with solvent or the caspase inhibitor (Z-VAD-FMK, 10 µmol/L; n=5 per group). *P<0.05, **P<0.01, ***P<0.001.