ATP converts necrosis to apoptosis in oxidant-injured endothelial cells

Lelli, Joseph L.; Becks, Lauren L.; Dąbrowska, Milena; Hinshaw, Daniel B.

doi:10.1016/s0891-5849(98)00107-5

Cited by 140 publications

(86 citation statements)

References 29 publications

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“…19,20 Defects in ATP synthesis, which might be due to failure in energy homeostasis, occurs at an early stage of necrosis, while a certain level of ATP synthesis can still be maintained until the late stages of apoptosis and autophagy. [21][22][23][24] Results from our lab revealed that axonal ATP levels start to decrease while the AMP level increases at early stages of Wallerian degeneration.…”

Section: Axon Degeneration and Cell Deathmentioning

confidence: 99%

NAD and axon degeneration: From the Wlds gene to neurochemistry

Wang¹,

He²

2009

Cell Adhesion & Migration

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Neurodegenerative diseases have become a global issue due to the aging population. These disorders affect a vast patient population and represent a huge area of unmet therapeutic need. Axon degeneration is a common pathological character of those neurodegenerative diseases. It results in the loss of communication between neurons. Two decades ago, the Wallerian degeneration slow (Wlds) mouse strain was identified, in which the degeneration of transected axons is delayed. The phenotype is attributed to the overexpression of a chimeric protein Wlds which contains a short fragment of the ubiquitin assembly protein UFD2 and the full-length nicotinamide adenine dinucleotide (NAD) synthetic enzyme Nicotinamide mononucleotide adenylyl-transferase-1 (Nmnat-1). However, the underlying molecular mechanism remains largely unknown. Recently, it's reported by independent researchers that the full length coding sequence of mouse Nmnat-1 could mimic the axonal protective effect of the Wlds gene when overexpressed in primary neural cultures. Together with a significant number of subsequential reports, this finding highlighted the substantial role of nicotinamide adenine dinucleotide (NAD) in the process of axon degeneration. Here we reviewed the history of axon degeneration research from a neurochemical standpoint and discuss the potential involvement of NAD synthesis, NAD consumption and NAD-dependent proteins and small molecules in axon degeneration.

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Section: Axon Degeneration and Cell Deathmentioning

confidence: 99%

NAD and axon degeneration: From the Wlds gene to neurochemistry

Wang¹,

He²

2009

Cell Adhesion & Migration

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“…Furthermore, the intracellular ATP level could be responsible for converting necrosis to apoptosis in oxidant-induced endothelial cell death [44]. Cell damage accompanies mitochondria membrane dysfunction not only in apoptosis but also in necrosis.…”

Section: Mitochondria Plays An Important Role In Apoptosis and Necrosmentioning

confidence: 99%

Glutathione depletion‐induced chromosomal DNA fragmentation associated with apoptosis and necrosis

Higuchi

2004

J Cellular Molecular Medi

181

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Chromosomal DNA and mitochondrial dysfunctions play a role on mammalian cell death induced by oxidative stress. The major biochemical dysfunction of chromosome is the presence of an ordered cleavage of the DNA backborn, which is separated and visualized as an electrophoretic pattern of fragments. Oxidative stress provides chromatin dysfunction such as single strand and double strand DNA fragmentation leading to cell death. More than 1 Mb of giant DNA, 200-800 kb or 50-300 kb high molecular weight (HMW) DNA and internucleosomal DNA fragments are produced during apoptosis or necrosis induced by oxidative stress such as glutathione (GSH) depletion in several types of mammalian cells. Reactive oxygen species (ROS)-mediated DNA fragmentation is enhanced by polyunsaturated fatty acids including arachidonic acid or their hydroperoxides, leading to necrosis. Mitochondrial dysfunction on decrease of trans membrane potential, accumulation of ROS, membrane permeability transition and release of apoptotic factors during apoptosis or necrosis has been implicated. This review refers to the correlation of chromosomal DNA fragmentation and apoptosis or necrosis induced by GSH depletion, and the possible mechanisms of oxidative stress-induced cell death.

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“…Apoptosis is known to be an active process requiring intracellular ATP (3,(32)(33)(34). In the absence of sufficient ATP, cells treated with toxic levels of various agents will die by necrosis instead of apoptosis (31,35).…”

Section: Modes Of Cell Death Induced In Burkitt's Lymphoma Cells By Vmentioning

confidence: 99%

Oxidative Stress Inhibits Apoptosis in Human Lymphoma Cells

Lee

Shacter

1999

Journal of Biological Chemistry

251

215

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Apoptosis and necrosis are two forms of cell death that are induced under different conditions and that differ in morphological and biochemical features. In this report, we show that, in the presence of oxidative stress, human B lymphoma cells are unable to undergo apoptosis and die instead by a form of necrosis. This was established using the chemotherapy drug VP-16 or the calcium ionophore A23187 to induce apoptosis in Burkitt's lymphoma cell lines and by measuring classical markers of apoptotic death, including cell morphology, annexin V binding, DNA ladder formation, and caspase activation. In the presence of relatively low levels of H 2 O 2 (75-100 M), VP-16 and A23187 were unable to induce apoptosis in these cells. Instead, the cells underwent non-apoptotic cell death with mild cytoplasmic swelling and nuclear shrinkage, similar to the death observed when they were treated with H 2 O 2 alone. We found that H 2 O 2 inhibits apoptosis by depleting the cells of ATP. The effects of H 2 O 2 can be overcome by inhibitors of poly(ADP)-ribosylation, which also preserve cellular ATP levels, and can be mimicked by agents such as oligomycin, which inhibit ATP synthesis. The results show that oxidants can manipulate cell death pathways, diverting the cell away from apoptosis. The potential physiological ramifications of this finding will be discussed.

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ATP converts necrosis to apoptosis in oxidant-injured endothelial cells

Cited by 140 publications

References 29 publications

NAD and axon degeneration: From the Wlds gene to neurochemistry

NAD and axon degeneration: From the Wlds gene to neurochemistry

Glutathione depletion‐induced chromosomal DNA fragmentation associated with apoptosis and necrosis

Oxidative Stress Inhibits Apoptosis in Human Lymphoma Cells

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