Cell death by apoptosis and its protective role against disease

Bursch, Wilfried; Oberhammer, Franziska; Schulte‐Hermann, Rolf

doi:10.1016/0165-6147(92)90077-j

Cited by 389 publications

(196 citation statements)

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“…Indeed, all criteria normally adopted to identify this process are met: inhibition of gene transcription and translation prevents the typical morphological (pyknosis) and biochemical (DNA fragmentation) hallmarks of apoptosis, and survival of ganglion cells is increased by this treatment. The criteria that we have selected in order to identify apoptotic cell death are among the most typical features of apoptosis (Bursch et al, 1992;Johnson and Dcckwerth, 1993).…”

Section: Discussionmentioning

confidence: 99%

Apoptotic cell death induced by optic nerve lesion in the neonatal rat

et al. 1994

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Cell death can be ascribed to one of two distinct modes of degeneration: apoptosis (programmed or active cell death) or necrosis (passive degeneration). While apoptosis is generally assumed to occur in physiological conditions such as normal development or tissue turnover, necrotic cell degeneration is induced in pathological situations. Here we report that also in a pathological situation, such as after axotomy in the CNS, apoptotic type of cell death comes into play: following intracranial transection of the optic nerve in the neonatal rat in vivo, retinal ganglion cells undergo an active, apoptotic cell death. In fact, the administration of protein synthesis inhibitors (actinomycin D and cycloheximide) prevents the appearance of pyknotic nuclei as well as of fragmented DNA of ganglion cells at 24 hr postlesion. Correspondingly, the number of surviving cells after actinomycin D and cycloheximide treatment is comparable to normal, unlesioned retinas. In addition, cycloheximide decreases the number of pyknotic ganglion cells during spontaneous cell death.

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Section: Discussionmentioning

confidence: 99%

Apoptotic cell death induced by optic nerve lesion in the neonatal rat

et al. 1994

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“…This finding is not surprising, given the quiescent state of this organ, in which there is no significant cell turnover. However, apoptosis may be induced in vivo in particular conditions, such as starvation, 23 liver regeneration after partial hepatectomy, 24 Pb nitrate administration, 25,26 during hepatocarcinogenesis, 27,28 or in vitro after transforming growth factor ␤ 1 treatment, 29 treatment with tumor necrosis factor ␣ following the addition of actinomycin D, 30 the use of microtubule-depolymerizing drugs, 31 or protein kinase C inhibitors. 32 Apoptotic events have never been described during liver morphogenesis, in contrast to other organs.…”

Section: Discussionmentioning

confidence: 99%

Retinoic acid treatment induces apoptosis or expression of a more differentiated phenotype on different fractions of cultured fetal rat hepatocytes

et al. 1998

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The present study reports the effects of retinoic acid (RA) on cultured fetal rat hepatocytes. We show that RA treatment induces both differentiation and apoptosis. Hepatocytes cultured for 48 hours in the presence of 5 mol/L RA form junctional complexes in the areas of contact between neighboring cells and develop bile canaliculi, typical features of mature and well-differentiated cells. At the same time, about 20% of cells are induced to die by apoptosis, and the percentage of apoptotic cells increases according to the concentration of RA used and the duration of treatment. The induction of apoptosis, studied at the morphological and biochemical levels, revealed that, in our system, the classical compaction of chromatin occurs only during the final stages of the process; instead of the common marker of apoptosis, i.e., the ''DNA ladder'' pattern of fragmentation, megabase-sized fragments were found. These observations provide further evidence of the existence of fundamental differences in the mechanisms of apoptosis among cell types. To investigate the molecular mechanism of the effects of RA, we evaluated the expression of two proteins, c-myc and p53, which are known to be involved in both cell differentiation and apoptosis. The data obtained show that the amount of p53 remained unchanged after RA treatment. On the contrary, a dose-dependent reduction in c-myc levels was found, suggesting that RA action may be mediated by modulation of this oncogene. Our findings regarding the apoptosis-inducing effect of RA, which was not found in adult hepatocytes, suggest a possible relationship between this phenomenon and the proliferative capacity and/or differentiation state of hepatocytes. (HEPATOLOGY 1998;28: 727-737.) Natural and synthetic retinoids, members of the vitamin A family, are compounds with numerous pleiotropic effects.

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“…Both necrosis 2,4 and apoptosis 27 have been suggested as the cause of cell death, and the CTL were supposed to be the main effectors. On the other hand, infiltration of NK cells seemed to inhibit the progress of various liver diseases, like hepatitis B, 3 while depressed NK activity was associated with development of liver carcinoma.…”

Section: Discussionmentioning

confidence: 99%

“…It is unclear whether hepatocytes in the diseased liver die by necrotic or apoptotic pathways. 2,4,27 Therefore, in the present study, we coincubated freshly isolated liver cells with IL-2-activated NK (A-NK) cells to study the mechanism of liver cell death. We found that NK cells induce activation of caspases, a decrease of mitochondrial membrane potential (MMP), formation of blebs, phosphatidyl serine (PS) externalization, and DNA fragmentation in hepatocytes indicative of apoptosis.…”

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confidence: 99%