Phospholipase C β3 deficiency leads to macrophage hypersensitivity to apoptotic induction and reduction of atherosclerosis in mice
J. Clin. Invest. Zhenglong Wang, et al. 118:195 doi:10.1172/JCI33139 [Go to this article.]

Figure 2
PLC β3 deficiency leads to an increased sensitivity of macrophages to apoptosis induction. (A–D) Increased apoptosis in macrophages from the 3-day thioglycolate-elicited model. (A) The numbers of peritoneal macrophages recovered from mice injected with thioglycolate for 3 days were counted (n = 27). (B) Percentages of macrophages with depolarized mitochondria (n = 4) were determined by FACS with the Mito-Probe dye and the anti-F4/80 antibody. (C) Percentages of annexin V–positive macrophages (n = 5) were determined by FACS analysis with annexin V and F4/80 antibodies. (D) Caspase-3 activity (n = 5) was determined using a caspase-3 assay kit from Roche Inc. (E–H) Increased sensitivity to apoptotic induction in macrophages from the 1-day thioglycolate–elicited model. Mice were injected with thioglycolate for 1 day, and percentages of macrophages with depolarized mitochondria (n > 4) were determined by FACS. For treatments, cells were incubated with 10 μg/ml 25-OHC, 100 μg/ml oxLDL, LPS (1 μg/ml)/CHX (1 μg/ml), or TNF-α (10 ng/ml)/CHX (10 μg/ml) for 24 hours. MT, mitochondria.