Showing papers on "Apoptosis published in 1984"

Chromatin cleavage in apoptosis: association with condensed chromatin morphology and dependence on macromolecular synthesis.

Abstract: In glucocorticoid-treated rat thymocytes and the murine lymphoid cell lines L5178 and S49 the morphology of apoptosis is associated with chromatin cleavage. The cleavage is at internucleosomal sites, apparently through activation of an endogenous endonuclease. In variants of the cell lines selected for resistance to glucocorticoid, neither apoptosis nor chromatin cleavage were observed after steroid treatment, and steroid receptors were undetectable. In thymocytes, both the morphological changes of apoptosis and chromatin cleavage were inhibited by cycloheximide and actinomycin D. The calcium-magnesium ionophore A23187 induced apoptosis and chromatin cleavage in thymocytes, and these effects were also inhibited by cycloheximide. The data confirm that the condensed chromatin which characterizes apoptosis morphologically consists of endogenously digested chromatin fragments. They also provide support for the view that at least some cells enter apoptosis by a process dependent upon macromolecular synthesis.

Cell death during differentiation of the retina in the mouse

Abstract: A reproducible pattern of cell death associated with differentiation of the retina in mice was analyzed quantitatively by microscopy. Cell death occurs primarily during the first 2 weeks after birth and is essentially complete by the end of the third week. Death of individual cells involves nuclear condensation and pyknosis (apoptosis), followed by phagocytosis of the cellular remains by adjacent cells or motile phagocytes. From birth through 4 days, an increasing incidence of cell death is observed among ventricular cells. Ganglion cell degeneration is prominent during the first 11 days, peaking on days 2-5. Many presumptive amacrine cells die within the inner plexiform and inner nuclear layers, particularly between 3 and 8 days. Among adjoining bipolar and Muller cells, degeneration reaches a peak at 8-11 days. On day 5, formation of the outer plexiform layer separates the rods into two groups. Rod nuclei situated on the inner side of that layer immediately move across it to enter the outer nuclear layer, but numerous cells die during nuclear migration. Sporadic death of rods continues during the following 2 weeks. Cell death associated with cell differentiation (histogenetic death) is considered to represent a normal developmental process. Possible mechanisms resulting in cell degeneration are discussed. It is suggested that genetically regulated cell death serves to fine-tune neuronal networks during the terminal stages of development.

Hormone-induced cell death. 2. Surface changes in thymocytes undergoing apoptosis.

Abstract: In vivo, apoptotic cells are swiftly recognized by phagocytes, presumably because of changes on their surface. This article describes surface changes in rat cortical thymocytes undergoing apoptosis induced by glucocorticoid treatment in vitro. Homogeneous populations of thymocytes early in apoptosis were prepared by isopyknic centrifugation. These cells were compared with purified nonapoptotic cells in terms of several surface characteristics, including binding to macrophages, surface ultrastructure, microelectrophoretic mobility (a measure of surface charge density), and ability to bind four lectins and four monoclonal antibodies to thymocyte antigens. Apoptotic cells bound to macrophages more avidly than did nonapoptotic cells by a process not dependent upon serum factors. Their surfaces lost microvilli and became " blistered ," apparently through fusion of vesicles of endoplasmic reticulum with the plasma membrane. The surface charge density of apoptotic cells was less than that of nonapoptotic cells. Surface antigens and lectin-binding sites were less abundant on apoptotic than on normal cells, in proportion to the general reduction in cell size observed in apoptosis. Differences between apoptotic and normal cells were not detected, however, in the relative quantities of exposed galactose, N-acetyl galactosamine, N-acetyl glucosamine, N-acetyl neuraminic acid, or of several surface antigens, including the major sialoglycoproteins of the thymocyte membrane. It appears that although several changes occur in the surface of apoptotic cells, many cell membrane structures remain intact. The changes responsible for the recognition of apoptotic cells by phagocytes are more subtle than those detectable by the binding of lectin and antibody probes, but preliminary data suggest that a lectin-sugar interaction is involved.

Occurrence of cell death (apoptosis) in preneoplastic and neoplastic liver cells. A sequential study.

Abstract: A sequential study was performed to investigate the occurrence of cell death in preneoplastic and neoplastic liver cells of F-344 rats. The animals were administered a single initiator dose of 1,2-dimethylhydrazine and were then subjected to a liver carcinogenesis promotion regimen, consisting of a diet containing 1% orotic acid. Cell death, morphologically similar to that described as apoptosis, was evident in foci of preneoplastic hepatocytes at 10 weeks after orotic acid feeding. An increased frequency of apoptotic bodies was observed in nodules, but not in the surrounding liver, 20 weeks after starting the dietary regimen, and in hepatocellular carcinomas that developed after 1 year of continuous promotion. Occurrence of this type of cell death was also observed in liver foci of rats subjected to two other promoting regimens, suggesting, thus, a possible relevance of apoptosis to the carcinogenic process in the liver.

Aberrant nuclear morphology in the mouse myeloma SP2/0 cell line.

Abstract: The mouse myeloma SP2/0 cell line when grown in supplemented Dulbecco's modified Eagle's media spontaneously produced aberrant nucleated cells which increased in frequency with cell culture age. These cells underwent cytological changes associated with apoptosis, that is, the condensation of chromatin followed by karyorrhexis and the production of small apoptotic bodies. Aberrant cells were induced by media changes, centrifugation, and temperature shocking. The rapid induction of aberrant cells by a media change suggests that the mechanism of fragmentation was not associated with cell division.