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. 2001 Jul 16;194(2):113–126. doi: 10.1084/jem.194.2.113

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© 2001 The Rockefeller University Press

This article is distributed under the terms of an Attribution–Noncommercial–Share Alike–No Mirror Sites license for the first six months after the publication date (see http://www.rupress.org/terms). After six months it is available under a Creative Commons License (Attribution–Noncommercial–Share Alike 4.0 Unported license, as described at http://creativecommons.org/licenses/by-nc-sa/4.0/).

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Caspase inhibitors do not prevent the loss of ΔΨ_m or macrophage PI uptake after PI3K/Akt-1 inhibition. Macrophages were treated with 100 μM zVAD.fmk, the caspase-9 inhibitor z-LEHD.fmk (100 μM) or control medium for 1 h, then 50 μM LY294002 was added for an additional 48 h. The cells were harvested and analyzed for mitochondrial retention of Rh123 (mean fluorescence, percentage of control; A), DNA fragmentation (% <2N DNA, B), PI uptake (percentage of PI-positive cells, C), caspase-9 activity (D), and the expression of proform of caspase-3 and full-length PKCδ (E). Each of the methods has been described previously. The results presented in each panel are representative of two or three experiments.

Caspase inhibitors do not prevent the loss of ΔΨ_m or macrophage PI uptake after PI3K/Akt-1 inhibition. Macrophages were treated with 100 μM zVAD.fmk, the caspase-9 inhibitor z-LEHD.fmk (100 μM) or control medium for 1 h, then 50 μM LY294002 was added for an additional 48 h. The cells were harvested and analyzed for mitochondrial retention of Rh123 (mean fluorescence, percentage of control; A), DNA fragmentation (% <2N DNA, B), PI uptake (percentage of PI-positive cells, C), caspase-9 activity (D), and the expression of proform of caspase-3 and full-length PKCδ (E). Each of the methods has been described previously. The results presented in each panel are representative of two or three experiments.