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 3
Ligand-induced PLC β3–dependent upregulation of Bcl-XL in macrophage and apoptosis protection. (A) One-day thioglycolate–elicited peritoneal macrophages were cultured in 10% FCS or charcoal-filtered FCS (CF-FCS) in the presence or absence of 300 nM S1P for 24 hours. Cells were then collected for Western blot analyses. Western blots from 3 experiments were quantified by densitometry. (B) Relative mRNA levels of Bcl-XL in 1-day thioglycolate–elicited peritoneal macrophages were determined by quantitative RT-PCR. (C) One-day thioglycolate–elicited PLC β3–null peritoneal macrophages were transfected with Bcl-XL expression plasmid using the Amaxa electroporation system. The next day, cells were treated with 25-OHC (2.5 μg/ml) for 24 hours and then stained with Mito-Probe. (D) Cells prepared and treated as in A were examined for their sensitivity to 25-OHC (10 μg/ml). (E and F) Cells prepared as in A were examined for their sensitivity to 25-OHC in the presence of 10% FCS or charcoal-filtered FCS containing SDF-1 (100 ng/ml), PAF (50 ng/ml), LPA (10 μM), or MCP (200 ng/ml). *P < 0.05 with versus without a ligand.