Activation of Human Neutrophils by the Anti-Inflammatory Mediator Esenbeckia leiocarpa Leads to Atypical Apoptosis
Figure 5
CHE increases the degradation of the cytoskeletal proteins gelsolin and paxillin but not vimentin during apoptosis. Cells were incubated (10 × 106 cells/mL) with the diluent (DMSO (1%, SA), Viscum album agglutinin-I (VAA) (1000 ng/mL) or 500 μg/mL CHE for 22 h. Degradation of gelsolin (Gel) (a), paxillin (Pax) (b), vimentin (Vim), or vinculin (Vinc) (c) was monitored by Western blot, as described in Section 2. Results are from one representative experiment of four. The position of the two paxillin fragments known to be recognized by the antibody (clone PXC-10) is illustrated. Bottom panels were stained with Coomassie blue at the end of the experiment in order to verify equivalent loading, except in (c), where the membranes were striped and probed with an antivinculin antibody for determining the equivalent loading. Note the appearance of the gelsolin fragment when cells were treated with VAA or CHE ((a), arrowhead).
