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. Author manuscript; available in PMC: 2010 Aug 17.
Published in final edited form as: J Mol Biol. 2005 Dec 20;356(4):876–885. doi: 10.1016/j.jmb.2005.12.006

Figure 3.

Figure 3

Anginex binds to and disrupts lipid bilayers. The binding of anginex to liposomes was assessed by measuring liposome-associated tryptophan fluorescence normalized for fluorescence intensity in the absence of liposomes. (a) Binding of anginex (10 μM) to zwitterionic DOPC liposomes (PC) occurred at millimolar phospholipid concentrations, whereas binding of anginex to anionic DOPS (PS) was saturated at approximately 100 μM lipid. Anginex binding to DOPS was ca fivefold higher than to DOPC:DOPS (8:2) liposomes (PCPS). (b) Binding of anginex to liposomes leads to the disruption of lipid bilayers as assessed by carboxyfluorescein (CF) dequenching. Anginex (AN) is more effective in releasing CF from DOPC:DOPG (PG) than from DOPC (PC) liposomes. A control peptide (CP) did not cause significant CF release from the DOPC:DOPG liposomes. (c) SubG1 analysis was performed by FACS after addition of liposomes to the HUVEC medium. Anginex-induced cell death (AN) was inhibited completely by anionic DOPC:DOPG liposomes (+PG). Zwitterionic DOPC liposomes reduced anginex cytotoxicity to HUVECs by approximately 30% (+PC). Results are presented as means and SEM (*p<0.05; **p<0.01).