Phagocytosis and degradation of rat liver mitochondria by cultivated human glial cells
Collins, V.P.; Arborgh, B.; Brunk, U.; Schellens, J.P.
Laboratory Investigation; A Journal of Technical Methods and Pathology 42(2): 209-216
1980
ISSN/ISBN: 0023-6837 PMID: 7354616 Document Number: 167575
Experimental induction of autophagocytosis usually involves cellular damage, which severely limits the possibility of drawing general conclusions from such systems. An experimental model was developed in which cells take up, by heterophagocytosis, material similar to that normally sequestered by autophagocytosis. Cultured glial cells were exposed to a suspension of rat liver mitochondria. The initial step of phagocytosis occurred along the edge or on the upper surface of the glial cells, usually in conjunction with microvilli and/or ruffle-like structures. Phagocytosis reached a peak after 12 h and declined after 48 h. Fusion of heterophagosomes with lysosomes was demonstrated by acid phosphatase cytochemistry and prior labeling of lysosomes with Thorotrast. The early stages of breakdown of mitochondria were characterized morphologically by fragmentation and an increase of flocculent densities; later, lysosomes were observed containing membrane fragments and irregular electron-dense material but no recognizable mitochondrial structures. By 14 days the volume density of residual bodies in the cytoplasm was significantly larger in mitochondria-exposed cells than in controls. The experimental model, whereby subcellular fractions containing material similar to that normally sequestered in autophagosomes are introduced into the lysosomal system by heterophagocytosis, is feasible and presents the possibility of studying the influence of an accumulation of residual bodies on cell metabolism.