LYSOSOMAL RESPONSES OF FETAL MOUSE HEARTS RECOVERING FROM ANOXIA AND SUBSTRATE DEPLETION
LYSOSOMAL RESPONSES OF FETAL MOUSE HEARTS RECOVERING FROM ANOXIA AND SUBSTRATE DEPLETION
复制标题
DOI：
10.1016/s0022-2828(86)80959-2
复制
发表时间：
1986-08-01
影响因子：
5
通讯作者：
DECKER, RS
中科院分区：
文献类型：
--
作者：
RIDOUT, RM;WILDENTHAL, K;DECKER, RS
从缺氧和底物剥夺的1小时期间的恢复是伴随着一个显着的溶酶体反应，保持在器官培养的胎鼠心脏的肌细胞。在恢复后5至15分钟内形成两类亚细胞空泡。一种似乎提供溶酶体酶降解亚细胞颗粒，而另一种分离受损肌细胞的细胞质内的细胞器。当两个群体相互融合时，被隔离的细胞器的降解似乎开始了。恢复6小时后，空泡内降解似乎完全，损伤的肌细胞在形态上与对照细胞无法区分，表明分区细胞器的分解是相当有效的。该过程可以继续进行，尽管速率降低，而蛋白质合成被抑制，因为放线菌酮仅适度干扰复氧后的恢复。本研究结果表明，胎鼠心脏的条件下，模拟缺血的一些重要方面是一个很好的模型，以检查溶酶体的作用，从亚致死性损伤的恢复过程中。
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.