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Showing papers on "Apoptosis published in 1987"


Journal ArticleDOI
TL;DR: During the involution of lead nitrate‐induced hyperplasia in rat liver a significant increase of transglutaminase activity, enzyme concentration, transglUTaminase messenger RNA and protein‐bound ε‐(γ‐glutamyl)lysine (product of transGlutaminases action) coincided with programmed death (apoptosis) of hepatocytes.

472 citations



Journal ArticleDOI
TL;DR: It is concluded that uterine epithelial cells surrounding mouse and rat embryos during implantation undergo apoptotic cell death leading to their phagocytosis by trophoblast cells.
Abstract: An ultrastructural study of mouse and rat embryo implantation sites was undertaken to determine whether the uterine luminal epithelial cells surrounding the blastocyst exhibited the morphologic characteristics of apoptotic or necrotic cell death. In both species the epithelial cells exhibited all of the characteristics of apoptosis, including surface blebbing, shrinkage and fragmentation of the cells, condensation of chromatin, and indentation and fragmentation of nuclei. Cytoplasmic organelles remained morphologically intact, and the cytoplasm maintained normal or increased staining density. Also, the epithelial cells and cell fragments were phagocytosed by the adjacent trophoblast cells. The epithelial cells did not exhibit the characteristics of necrotic cell death, such as swollen cells and mitochondria, damaged surface membranes, and disintegrated cytoplasmic organelles. We conclude that uterine epithelial cells surrounding mouse and rat embryos during implantation undergo apoptotic cell death leading to their phagocytosis by trophoblast cells.

199 citations


Book ChapterDOI
TL;DR: A concept of cell death is presented which differs from, but complements, the classical toxicological view and is seen to be mediated by cer­tain intracellular events, which can be defined in molecular terms, and which are themselves internally regulated.
Abstract: The purpose of this paper is to present a concept of cell death which differs from, but complements, the classical toxicological view. Evidence will be reviewed which shows that cells can (and in most cases eventually do) die in response to physiological stimuli. Physiological cell death will be seen to be mediated by cer­tain intracellular events, which can be defined in molecular terms, and which are themselves internally regulated.

97 citations


Journal Article
TL;DR: It is proposed that cell death may be as important as cell proliferation in the regulation of normal uterine epithelial growth in the rabbit endometrial epithelium.
Abstract: It is known that estrogen (E) and progesterone (P) play important roles in the regulation of endometrial growth. In the rabbit endometrial epithelium, a balance is maintained between cell proliferation and cell death which seems to be under ovarian hormonal control. In this study the authors determined cell proliferation by quantitating the mitotic index (MI) and cell death by quantitating the death index (DI) in uterine histologic sections from whole animals that were hormone treated versus control rabbits. E caused proliferation of uterine epithelial cells and decreased the DI transiently, while P also increased proliferation but decreased the DI dramatically. In a time course study, after a single injection of human chorionic gonadotropin to induce pseudopregnancy, there was transient decrease in the DI and an increase in the MI between Days 2 and 5. In pseudopregnant animals, hormones had no effect in intact animals, but after ovariectomy there was about a 124-fold increase in the DI, which could be prevented by P administration. The predominant type of cell death observed in this system is apoptosis (97.5%), as opposed to necrosis (2.5%). Thus, it is proposed that cell death may be as important as cell proliferation in the regulation of normal uterine epithelial growth.

93 citations


Journal ArticleDOI
TL;DR: Chinese hamster V79 fibroblast cells were exposed to brief periods of cold but non-freezing temperatures at different points on the population growth curve and apoptosis was expressed, suggesting that cold shock served as a stimulus for susceptible cells to undergo apoptosis.

69 citations


Journal ArticleDOI
TL;DR: Part of the biochemical explanation for this onset of cell death comes from the accelerated loss from the tissue of estriol when compared to estradiol-17β, which resulted in a decline in protein and rRNA biosynthesis and a failure to complete ribosomal maturation.
Abstract: The luminal epithelium of adult ovariectomized mice responds to estradiol-17β with a synchronised wave of DNA synthesis and mitosis. Estriol, however, although producing a similar DNA-synthetic and mitotic response fails to cause an increase in cell number owing to a wave of cell death occurring at mitosis. In the present study it was shown that cells died by two different routes. The majority died by apoptosis but, unusually, a minority also died by necrosis. In the apoptotic cells the cytoplasm became dense, the endoplasmic reticulum and nuclear cisternae dilated; chromatin became marginated the nucleus shrank and became deeply infolded and contorted. Apoptosis, however, was uncharacteristic in that the nucleus failed to fragment, form caps or show disruption before the cells died by membrane rupture. Furthermore, the cells were frequently lost in sheets from the epithelium into the lumen. Part of the biochemical explanation for this onset of cell death comes from the accelerated loss from the tissue of estriol when compared to estradiol-17β. This resulted in a decline in protein and rRNA biosynthesis and a failure to complete ribosomal maturation. Evidence in favour of this explanation came from experiments that showed a return to the estradiol-17β level of response and an inhibition of cell death when the occupancy of the estriol receptor was maintained.

66 citations


Journal Article

16 citations


Journal ArticleDOI
TL;DR: Electron microscopic studies of acidophilic or Councilman‐like bodies in the liver show that they are manifestations of apoptosis, and the morphology and biochemistry suggest a process of active cellular self‐destruction rather than degeneration.

11 citations