Lysosomal responses of fetal mouse hearts recovering from anoxia and substrate depletion.
Recovery from a 1 h period of anoxia and substrate deprivation is accompanied by a marked lysosomal response in myocytes of fetal mouse hearts maintained in organ culture. Two classes of subcellular vacuoles form within 5 to 15 min of recovery. One appears to provide lysosomal enzymes for degradation of subcellular particles, while the other segregates organelles within the cytoplasm of the injured myocyte. When the two populations fuse with each other, the degradation of sequestered organelles appears to commence. After 6 h of recovery, intravacuolar degradation appears complete, and the injured myocytes are morphologically indistinguishable from control cells, demonstrating that the breakdown of the partitioned cell organelles is quite efficient. The process can proceed, albeit at a reduced rate, while protein synthesis is inhibited, since cycloheximide only modestly interferes with recovery after reoxygenation. The present results demonstrate that the fetal mouse heart subjected to conditions that simulate some important aspects of ischemia is an excellent model to examine the role of lysosomes during recovery from sublethal injury.
D000818:Animals; D002401:Cathepsin B; D002402:Cathepsin D / Q000378:metabolism; D002403:Cathepsins / Q000378:metabolism; D005260:Female; D005333:Fetus; D000860:Hypoxia / Q000378:metabolism*; D008247:Lysosomes / Q000378:metabolism* / Q000648:ultrastructure; D051379:Mice; D008854:Microscopy, Electron; D009206:Myocardium / Q000378:metabolism* / Q000648:ultrastructure; D009924:Organ Culture Techniques; D011247:Pregnancy; D014176:Protein Biosynthesis
D002403:Cathepsins; D002401:Cathepsin B; D002402:Cathepsin D