Apoptosis, Pyroptosis, and Necrosis: Mechanistic Description of Dead and Dying Eukaryotic Cells

Fink, Susan L.; Cookson, Brad T.

doi:10.1128/iai.73.4.1907-1916.2005

Cited by 1,844 publications

(1,538 citation statements)

References 143 publications

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“…Pyroptosis is an inflammatory, caspase-1-dependent, programmed cell death mechanism distinct from apoptosis and oncosis in that pyroptosis: (a) does not depend on the effector caspases-3, 6, and 7 that trigger apoptosis; (b) is inhibited with the selective caspase-1 inhibitor peptide tyrosine-valine-alanine-aspartic acid (YVAD); (c) results in 1 to 2 nm pores in the plasma membrane with lysis of the cell and release of its proinflammatory contents; and (d) progresses with an intact mitochondria. 1 The proinflammatory effects of pyroptotic cell death are due in part to the maturation and release of interleukin-1b (IL-1b).…”

Section: Introductionmentioning

confidence: 99%

Pyroptotic Neuronal Cell Death Mediated by the AIM2 Inflammasome

Adamczak

Vaccari

Dale

et al. 2014

J Cereb Blood Flow Metab

251

237

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The central nervous system (CNS) is an active participant in the innate immune response to infection and injury. In these studies, we show embryonic cortical neurons express a functional, deoxyribonucleic acid (DNA)-responsive, absent in melanoma 2 (AIM2) inflammasome that activates caspase-1. Neurons undergo pyroptosis, a proinflammatory cell death mechanism characterized by the following: (a) oligomerization of apoptosis-associated speck-like protein containing a caspase recruitment domain (ASC); (b) caspase-1 dependency; (c) formation of discrete pores in the plasma membrane; and (d) release of the inflammatory cytokine interleukin-1b (IL-1b). Probenecid and Brilliant Blue FCF, inhibitors of the pannexin1 channel, prevent AIM2 inflammasome-mediated cell death, identifying pannexin1 as a cell death effector during pyroptosis and probenecid as a novel pyroptosis inhibitor. Furthermore, we show activation of the AIM2 inflammasome in neurons by cerebrospinal fluid (CSF) from traumatic brain injury (TBI) patients and oligomerization of ASC. These findings suggest neuronal pyroptosis is an important cell death mechanism during CNS infection and injury that may be attenuated by probenecid.

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Section: Introductionmentioning

confidence: 99%

Pyroptotic Neuronal Cell Death Mediated by the AIM2 Inflammasome

Adamczak

Vaccari

Dale

et al. 2014

J Cereb Blood Flow Metab

251

237

View full text Add to dashboard Cite

show abstract

“…Cell death is classified into necrosis and apoptosis according to morphological and biochemical characteristics (Fink et al 2005). Necrosis is caused by large environmental deviations from cellular homeostasis, such as ischemia or injury, and is associated with disruption of the cell membrane.…”

Section: Discussionmentioning

confidence: 99%

Activation of caspase 3, 9, 12, and Bax in masseter muscle of mdx mice during necrosis

Honda

Abe

Hiroki

et al. 2007

J Muscle Res Cell Motil

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The mdx mouse, a model of muscular dystrophy, lacks dystrophin, a cell membrane protein. It is known that the lack of dystrophin causes muscle fiber necrosis from 2 weeks after birth, and the majority of necrotic muscle fibers are replaced by regenerated muscle fibers by 4 weeks after birth. A recent study indicated the possibility that mitochondria-mediated intracellular stress, a phenomenon similar to apoptosis, may be produced during muscle fiber necrosis, but did not analyze endoplasmic reticulum-mediated intracellular stress.Therefore, we examined the expression of the caspase-12 gene involved in the endoplasmic reticulum stress pathway and the Bax, caspase-9, and caspase-3 genes involved in the mitochondrial stress pathway in the mdx masseter muscle. We found over-expression of caspase-12 in cells at 2-3 weeks after birth when muscle fiber necrosis was not prominent. This suggests that s tress occurs in the endoplasmic reticulum to maintain cell morphology in the absence of dystrophin. In addition, Bax was abundantly expressed in the mdx masseter muscle at 3 weeks after birth, and the expression of caspase-9 and -3 was prominent at 3-4 weeks after birth when necrosis and regeneration were marked. These results indicate that endoplasmic reticulum and mitochondrial stresses are produced during necrosis of 3 the mdx masseter muscle, and suggest that these events are a phenomenon similar to apoptosis.

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“…A variety of cellular signaling pathways regulates apoptosis, which is characterized morphologically by nuclear fragmentation, cleavage of chromosomal DNA into internucleosomal fragments, packaging of cellular debris into 'apoptotic bodies' without plasma membrane breakdown and exposure of surface molecules targeting the cell remnants for phagocytosis. 1,2 Major signaling pathways leading to apoptosis involve the activation of cystein-dependent, aspartate-directed proteases termed caspases. Depending on the type of stimuli and/or cell type, the apoptotic cascade can follow either an intrinsic pathway, involving apoptogenic mitochondrial proteins such as cytochrome c, or an extrinsic pathway that follows activation of a death receptor.…”

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confidence: 99%

“…Autophagic cells exhibit vacuolization, degradation of cytoplasmic contents and slight chromatin condensation; the molecular mechanisms regulating autophagy are now being elucidated. 2,3 Mechanisms of apoptosis specific to the lungs The topic of apoptosis and its regulation in the lungs has been reviewed recently; 4 this section will briefly summarize apoptosis mechanisms specific to acute respiratory distress syndrome (ARDS), chronic obstructive pulmonary disease (COPD) and pulmonary fibrosis (PF) that may be relevant to meconium aspiration syndrome (MAS).…”

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confidence: 99%

Angiotensin II in apoptotic lung injury: potential role in meconium aspiration syndrome

Uhal

Abdul-Hafez

2008

J Perinatol

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Meconium aspiration injures a number of cell types in the lung, most notably airway and alveolar epithelial lining cells. Recent data show that at least some of the cell death induced by meconium occurs by apoptosis, and therefore has the potential for pharmacologic inhibition through the use of apoptosis blockers or other strategies. Related work in adult animal models of lung injury has shown that apoptosis of lung epithelial cells induces a local (that is, entirely lung tissue specific) renin-angiotensin system (RAS L ). Furthermore, this inducible RAS L is required for the apoptotic response and affects other adjacent cell types through the release of angiotensin II and related peptides. This manuscript reviews the published data supporting this viewpoint as well as more recent works that suggest the involvement of a RAS L in the perinatal lung damage associated with meconium aspiration syndrome (MAS). The implications of these findings regarding their potential for the clinical management of MAS are also discussed.

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Apoptosis, Pyroptosis, and Necrosis: Mechanistic Description of Dead and Dying Eukaryotic Cells

Cited by 1,844 publications

References 143 publications

Pyroptotic Neuronal Cell Death Mediated by the AIM2 Inflammasome

Pyroptotic Neuronal Cell Death Mediated by the AIM2 Inflammasome

Activation of caspase 3, 9, 12, and Bax in masseter muscle of mdx mice during necrosis

Angiotensin II in apoptotic lung injury: potential role in meconium aspiration syndrome

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