Electron microscopical studies on the degradation of the apical ridge during the development of limbs in rat embryos

Schweichel, J.-U.

doi:10.1007/bf00519177

Cited by 22 publications

(6 citation statements)

References 25 publications

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“…Although programmed cell death (pcd) has often been equated with apoptosis, it has become increasingly clear that non-apoptotic forms of pcd also exist [6][7][8][9][10][11][12][13][14][15][16][17]. For example, certain developmental cell deaths, such as "autophagic" cell death [4,6,[13][14][15] and "cytoplasmic" cell death [6,7,[10][11][12]15], appear to be non-apoptotic. Furthermore, neurodegenerative diseases such as Huntington's disease and amyotrophic lateral sclerosis demonstrate neuronal cell deaths that do not fulfill the criteria for apoptosis [8,17].…”

Section: Cell Death: Background and Me-chanistic Taxonomymentioning

confidence: 99%

Programmed Cell Death Mechanisms in Neurological Disease

Bredesen

2008

CMM

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Programmed cell death (pcd) is a form of cell death in which the cell plays an active role in its own demise. Pcd plays a critical role in the development of the nervous system, as well as in its response to insult. Both anti-pcd and pro-pcd modulators play prominent roles in development and disease, including neurodegeneration, cancer, and ischemic vascular disease, among others. Over 100,000 published studies on one form of programmed cell death-apoptosis-have appeared, but recent studies from multiple laboratories suggest the existence of non-apoptotic forms of programmed cell death, such as autophagic programmed cell death. In addition, there appear to be programmatic cell deaths that do not fit the criteria for either apoptosis or autophagic cell death, arguing that additional programs may also be available to cells. Constructing a mechanistic taxonomy of all forms of pcd-based on inhibitors, activators, and identified biochemical pathways involved in each form of pcd-should offer new insight into cell deaths associated with various disease states, and ultimately offer new therapeutic approaches.

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Section: Cell Death: Background and Me-chanistic Taxonomymentioning

confidence: 99%

Programmed Cell Death Mechanisms in Neurological Disease

Bredesen

2008

CMM

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“…In an ultrastructural study of various tissues from embryonic and fetal rats and mice, Schweichel and Merker (1973; see also Schweichel 1972) proposed that there are three main types of cell death in developing tissues. A fundamental distinction between the three was seen to lie in the role of the lysosomes.…”

Section: A Morphological Types Of Dying Cellsmentioning

confidence: 99%

“…Schweichel and Merker found that this type of cell death occurred in almost all isolated dying cells, but never in regions of wholcsale destruction. They observed it in many different regions including the apical ectodermal ridge (Schweichel 1972) and parts of the nervous system. However, the identification of the dying cells in the apical ectodermal ridge as type 1 does not agree with an earlier report (Jurand 1965) in which they had many of the properties of type 2 (autophagic) dying cells (see below).…”

Section: A Morphological Types Of Dying Cellsmentioning

confidence: 99%

Developmental cell death: morphological diversity and multiple mechanisms

1990

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Physiological cell death is a widespread phenomenon in the development of both vertebrates and invertebrates. This review concentrates on an aspect of developmental cell death that has tended to be neglected, the manner in which the cells are dismantled. It is emphasized that the dying cells may adopt one of at least three different morphological types: "apoptotic", "autophagic", and "non-lysosomal vesiculate". These probably reflect a corresponding multiplicity of intracellular events. In particular, the destruction of the cytoplasm in these three types appears to be achieved primarily by heterophagy, by autophagy and by non-lysosomal degradation, respectively. The various mechanisms underlying both nuclear and cytoplasmic destruction are reviewed in detail. The multiplicity of destructive mechanisms needs to be born in mind in studies of other aspects of cell death such as the signals which trigger it, since different signals probably trigger different types of cell death.

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“…A list of the genes whose expression presented a mean log 2 ratio (experimental/reference) of Ն0.6, with a coefficient of variance (COV ϭ S.D./ mean log 2 ratio) of Ͻ30% were included, giving a total of 91 differentially regulated genes out of 7483. 1 R is a G-protein-coupled receptor that is connected by various second messengers to a wide variety of effector mechanisms to modulate cellular function. Three apparently independent second messenger systems can be activated by G-proteins following ligand binding to NK 1 R: 1) Ca 2ϩ mobilization from both intra-and extracellular sources via stimulation of phospholipase C; 2) arachidonic acid mobilization via phospholipase A2; and 3) cAMP accumulation via stimulation of adenylate cyclase (25).…”

Section: Microarray Data Acquisition and Analysismentioning

confidence: 99%

“…agic" cell death (1)(2)(3)(4)(5) and "cytoplasmic" cell death (2, 4, 6 -9), do not resemble apoptosis. Furthermore, neurodegenerative diseases such as Huntington's disease and amyotrophic lateral sclerosis demonstrate neuronal cell death that does not fulfill the criteria for apoptosis (10,11) but instead resembles a recently described form of pcd dubbed paraptosis (12).…”

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confidence: 99%

Alternative, Nonapoptotic Programmed Cell Death

Castro-Obregón

Rao

Río

et al. 2004

Journal of Biological Chemistry

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Programmed cell death (pcd) may take the form of apoptosis or of nonapoptotic pcd. Whereas cysteine aspartyl-specific proteases (caspases) mediate apoptosis, the mediators of nonapoptotic cell death programs are much less well characterized. Here we report that alternative, nonapoptotic pcd induced by the neurokinin-1 receptor (NK 1 R) activated by its ligand Substance P, is mediated by a MAPK phosphorylation cascade recruited by the scaffold protein arrestin 2. The activation of the protein kinases Raf-1, MEK2, and ERK2 is essential for this form of nonapoptotic pcd, leading to the phosphorylation of the orphan nuclear receptor Nur77. NK 1 Rmediated cell death was inhibited by a dominant negative form of arrestin 2, Raf-1, or Nur77, by MEK1/2-specific inhibitors, and by RNA interference directed against ERK2 or MEK2 but not ERK1 or MEK1 and against Nur77. The MAPK pathway is also activated in neurons in primary culture undergoing NK 1 R-mediated death, since the MEK inhibitor PD98059 inhibited Substance P-induced death in primary striatal neurons. These results suggest that Nur77, which is regulated by a MAPK pathway activated via arrestin 2, modulates NK 1 R-mediated nonapoptotic pcd.

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Electron microscopical studies on the degradation of the apical ridge during the development of limbs in rat embryos

Cited by 22 publications

References 25 publications

Programmed Cell Death Mechanisms in Neurological Disease

Programmed Cell Death Mechanisms in Neurological Disease

Developmental cell death: morphological diversity and multiple mechanisms

Alternative, Nonapoptotic Programmed Cell Death

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