|
|
|
|
|
|
|
|
|||||
| Home Help Feedback Subscriptions Archive Search Table of Contents | |||||
|
Fig. 1. Distinct morphological features of apoptosis, necrosis and autophagy. Immortal baby mouse kidney epithelial (iBMK) cell lines competent for apoptosis (wild-type), necrosis (apoptosis-defective and autophagy disabled by AKT activation) and autophagy (apoptosis defective) (Degenhardt et al., 2002; Degenhardt et al., 2006; Degenhardt and White, 2006) were subjected to metabolic stress (ischemia) for up to five days. Morphological changes were observed by time-lapse microscopy (100x). Representative individual cells from each cell line were followed for the indicated times, beginning immediately prior to any signs of altered morphology in metabolic stress (13.5 hours for wild-type, 16.6 hours for apoptosis- and autophagy-defective and 52.6 hours for apoptosis-defective cells). Cells undergoing apoptosis or necrosis are not viable at the end of each specified time, whereas cells capable of autophagy by virtue of an apoptotic defect retained viability for more than five days (Degenhardt et al., 2006). Following 112 hours of metabolic stress, apoptosis-defective cells that underwent autophagy were returned to normal culture conditions and photographed to document recovery (Degenhardt et al., 2006). The majority of these cells were able to recover and proliferate upon restoration of nutrients, and a representative cell is shown. Reproduced in part from Degenhardt et al. (Degenhardt et al., 2006) with permission from Elsevier.
|
