Cell death in health and disease: the biology and regulation of apoptosis

Bellamy, Christopher; Malcomson, Roger D. G.; Harrison, David J.; Wyllie, A.H.

doi:10.1006/scbi.1995.0002

Cited by 227 publications

(151 citation statements)

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“…42 These cellular changes were not evident in the monolayers treated with U18666A plus an ACAT inhibitor or with U18666A alone or in the control cells. Cell death is not easy to quantify except in synchronized cultures; thus, elaborate schemes have been devised to precisely quantify the extent of cell death.…”

Section: Cell Death and Apoptosismentioning

confidence: 89%

Effects of Intracellular Free Cholesterol Accumulation on Macrophage Viability

Kellner-Weibel

Jerome

Small

et al. 1998

ATVB

156

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Abstract-This study was designed to identify cellular responses associated with free cholesterol (FC) accumulation in model macrophage foam cells. Mouse peritoneal macrophages (MPMs) or J774 macrophages were loaded with cholesteryl esters using acetylated LDL and FC/phospholipid dispersions and were subsequently exposed to an acyl coenzyme A:cholesterol acyltransferase (ACAT) inhibitor. This treatment produced a rapid accumulation of cellular FC. The FC that accumulated due to ACAT inhibition was more readily available for efflux to 2-hydroxypropyl-␤-cyclodextrin (which removes cholesterol from the plasma membrane) than FC in untreated control cells. After a 3-hour exposure to an ACAT inhibitor, a significant increase in phospholipid synthesis was seen, followed by the leakage of LDH after 12 hours of treatment.

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Section: Cell Death and Apoptosismentioning

confidence: 89%

Effects of Intracellular Free Cholesterol Accumulation on Macrophage Viability

Kellner-Weibel

Jerome

Small

et al. 1998

ATVB

156

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“…[27][28][29][30][31][32] . Bcl-2 in an apoptosisrelated gene and plays an important role in regulating apoptosis [33][34][35][36][37][38] , by blocking the final pathway of apoptotic signal transmitted system [39][40][41][42][43][44] . Bcl-2 can inhibit the apoptosis stimulated by chemotherapeutic drugs, radiotherapy, heat shock, free radicals, Ca 2+ and TNF etc.…”

Section: Discussionmentioning

confidence: 99%

Effect of arsenic trioxide on human hepatoma cell line BEL-7402 culturedin vitro

Xu¹

2000

WJG

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AIMTo study the effect of a varying concentrations of arsenic trioxide on human hepatoma cell line BEL-7402 cultured in vitro and its mechanism of action. METHODS The BEL-7402 cells were treated with arsenic trioxide (at the concentrations of 0.5,1,2µ µ µ µ µmol/L, respectively) for 4 successive days. The cell growth and proliferation were observed by cell counting and cell-growth curve. Morphologic changes were studied with electronmicroscopy. Flow cytometry was used to assay cell-DNA distribution and the protein expression of Bcl-2 and Bax detected by immuno cytochemical method. RESULTS The cell growth was significantly inhibited by varying concentrations of arsenic trioxide as revealed by cell counting and cellgrowt h curve, which was dose-and timedependent. Arsenic trioxide treatment at 0.5, 1 and 2µ µ µ µ µmol/L resulted in a sub G1 cell peak, the apoptosis rate of the control group was 9.31% and that of 0.5µ µ µ µ µmol/L arsenic trioxide 15.53%, no significant difference was seen between the two. The apoptosis rates of 1, 2µ µ µ µ µmol/L arsenic trioxide were 19.10% and 21.87% respectively, which were much higher (both P<0.05). Decrease of G 0 /G 1 phase cells and increase of S phase cells were observed by flow cytometry, suggesting the inhibition effect of 0.5, 1, 2µ µ µ µ µmol/L arsenic trioxide on BEL-7402 cell lay in the G 0 /G 1 phase. Morphologic changes such as intact cell membrane, nucleic condensation, apoptotic body formation were seen under transmission electronmicrescopy, whereas the 0.5mol/L arsenic trioxide-treated BEL-7402 cells showed decrease of nucleocytoplasmic ratio, round nucleus, well-differentiated organelles in the cytoplasm. The processes and microvilli on the cell surface of the experimental groups under scanning electron microscopy were significantly decreased. High expressions of Bcl-2 and Bax were detected in 1 and 2µ µ µ µ µmol/L arsenic trioxide-treated cells, these were 46%, 87.33% and 83.08%, 95.83% respecti vely, among which that of Bax was more significant. Arsenic trioxide treatment at 0.5µ µ µ µ µmol/L resulted in a higher expression level of Bcl-2 and lower expression level of Bax, which were 8.81% and 3.83% respectively, as compared with that of the control group (15.33%) (P 1 <0.01, P 2 <0.01). CONCLUSIONArsenic trioxide not only inhibited proliferation but also induced apoptosis of human hepatoma cell line BEL-7402. The induced-apoptosis effect of 1, 2µ µ µ µ µmol/L arsenic trioxide was related to the expression level of Bcl-2 and Bax.

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“…Apoptosis is highly coordinated and is generally thought to be mediated by active intrinsic mechanisms, although extrinsic factors can contribute (16,30,205). Apoptosis is genetically controlled and is defined by cytoplasmic and nuclear shrinkage, chromatin margination and fragmentation, and breakdown of the cell into multiple spherical bodies that retain membrane integrity (25,101,138,246).…”

Section: Modes Of Cell Deathmentioning

confidence: 99%

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

Padanilam

2003

American Journal of Physiology-Renal Physiology

330

268

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In humans and experimental models of renal ischemia, tubular cells in various nephron segments undergo necrotic and/or apoptotic cell death. Various factors, including nucleotide depletion, electrolyte imbalance, reactive oxygen species, endonucleases, disruption of mitochondrial integrity, and activation of various components of the apoptotic machinery, have been implicated in renal cell vulnerability. Several approaches to limit the injury and augment the regeneration process, including nucleotide repletion, administration of growth factors, reactive oxygen species scavengers, and inhibition of inducers and executioners of cell death, proved to be effective in animal models. Nevertheless, an effective approach to limit or prevent ischemic renal injury in humans remains elusive, primarily because of an incomplete understanding of the mechanisms of cellular injury. Elucidation of cell death pathways in animal models in the setting of renal injury and extrapolation of the findings to humans will aid in the design of potential therapeutic strategies. This review evaluates our understanding of the molecular signaling events in apoptotic and necrotic cell death and the contribution of various molecular components of these pathways to renal injury.

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Cell death in health and disease: the biology and regulation of apoptosis

Cited by 227 publications

References 0 publications

Effects of Intracellular Free Cholesterol Accumulation on Macrophage Viability

Effects of Intracellular Free Cholesterol Accumulation on Macrophage Viability

Effect of arsenic trioxide on human hepatoma cell line BEL-7402 culturedin vitro

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

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