FIGURE 7.

Lipid membrane permeabilization caused by SAA prefibrillar oligomers. a, membrane leakage or disruption by SAA aggregates was probed by measuring the conductance across the lipid bilayer. SAA2.2 oligomers interacted with the lipid bilayer and caused membrane disruption at 0 h and membrane leakage at 1 h, but no membrane interaction was observed with older aggregates. b, SAA1.1 oligomers formed within 24 h caused membrane leakage or complete membrane disruption, but no leakage was observed for the 2-week sample. c, kinetics of SAA2.2 and SAA1.1 membrane permeabilization were probed using a calcein-based liposome leakage assay. SAA1.1 oligomers showed a higher propensity to cause liposome disruption and for a longer period of time relative to SAA2.2 oligomers. Mature amyloid fibrils of both SAA1.1 and SAA2.2 caused lower membrane leakage relative to their respective oligomers. d, the effect of various SAA aggregates on HEK293 cell was monitored using cell viability (MTS reduction) assay. SAA aggregates were added to cell cultures at a final concentration of 0.3 mg/ml and incubated at 37 °C for 6, 24, and 72 h before determining cell viability. Cell viability is expressed as the percentage reduction of MTS in treated cells compared with cells not exposed to any treatment (Live). Killed cells are those wells where media were replaced by sterile water. The error bars in represent the S.D. from two independent experiments.