Developmental cell death: morphological diversity and multiple mechanisms

Clarke, Peter G. H.

doi:10.1007/bf00174615

Cited by 1,536 publications

(1,163 citation statements)

References 125 publications

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“…Per haps an ischemic insult dissociates these two phe nomena by being so massive that it overwhelms the normal apoptotic removal systems, and the dying neuron disintegrates so fast that it never displays the nuclear condensation normally seen linked in developmental programmed cell death. It must also be cautioned that attempts to shoehorn all neuronal death into either necrosis or apoptosis ignore sug gestions that are multiple and diverse ways for cells to degenerate (Clarke, 1990;Schwartz et al, 1993). We conclude that transient forebrain ischemia produces ordered fragmentation of chromatin even many days after the precipitating ischemic insult, whereas random events predominate in the frankly pan-necrotic tissue.…”

Section: N H S N H Sn Hs N H Smentioning

confidence: 79%

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

MacManus¹,

Hill²,

Preston³

et al. 1995

J Cereb Blood Flow Metab

113

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Summary:The time course of appearance of cells with DNA damage was studied in rats following transient se vere forebrain ischemia. This DNA damage could be de tected by in situ end-labeling on brain sections. The breaks in DNA appeared selectively by day I in the stri atum and later in the CAl region of the hippocampus. It was possible by double labeling to show that there was no DNA damage in astrocytes. The DNA breaks consisted of laddered DNA fragments indicative of an ordered ap optotic type of internucleosomal cleavage, which per sisted without smearing for up to 7 days of reperfusion. In

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Section: N H S N H Sn Hs N H Smentioning

confidence: 79%

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

MacManus¹,

Hill²,

Preston³

et al. 1995

J Cereb Blood Flow Metab

113

View full text Add to dashboard Cite

show abstract

“…Apoptosis is characterized by cell rounding, membrane blebbing, cytoskeletal collapse, nuclear pyknosis, chromatin condensation/fragmentation and the formation of membrane-bound apoptotic bodies (Kerr et al, 1972;Wyllie et al, 1980;Clarke, 1990). These bodies are rapidly phagocytosed and digested by macrophages or neighboring cells.…”

Section: Introductionmentioning

confidence: 99%

Chronic UVA irradiation of human HaCaT keratinocytes induces malignant transformation associated with acquired apoptotic resistance

Huang

et al. 2006

Oncogene

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Ultraviolet A (UVA, 315-400 nm), constituting about 95% of ultraviolet irradiation in natural sunlight, represents a major environmental challenge to the skin and is clearly associated with human skin cancer. It has proven difficult to show direct actions of UVA as a carcinogen in human cells. Here, we demonstrate that chronic UVA exposures at environmentally relevant doses in vitro can induce malignant transformation of human keratinocytes associated with acquired apoptotic resistance. As evidence of carcinogenic transformation, UVAlong-treated (24 J/cm 2 once/week for 18 weeks) HaCaT (ULTH) cells showed increased secretion of matrix metalloproteinase (MMP-9), overexpression of keratin 13, altered morphology and anchorage-independent growth. Malignant transformation was established by the production of aggressive squamous cell carcinomas after inoculation of ULTH cells into nude mice (NC r -nu). ULTH cells were resistant to apoptosis induced not only by UVA but also by UVB and arsenite, two other human skin carcinogens. ULTH cells also became resistant to apoptosis induced by etoposide, staurosporine and doxorubicin hydrochloride. Elevated phosphorylation of protein kinase B (PKB, also called AKT) and reduced expression of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) were detected in ULTH cells. The resistance of ULTH cells to UVA-induced apoptosis was reversed by either inhibition of phosphatidylinositol 3-kinase (PI-3K) or adenovirus expression of PTEN or dominant negative AKT. These data indicate that UVA has carcinogenic potential in human keratinocytes and that the increased AKT signaling and decreased PTEN expression may contribute to this malignant transformation. Further comparisons between the transformed ULTH and control cells should lead to a better understanding of the mechanism of UVA carcinogenesis and may help identify biomarkers for UVA-induced skin malignancies.

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“…Programmed cell death (PCD) has long been proposed to participate in the morphogenesis of different organs and tissues (Clarke, 1990;Glucksmann, 1951;Saunders, 1966). The amniote limb is a classic model for studying the mechanisms that control cell death during embryogenesis, with the majority of the descriptive and experimental work performed in chick limbs.…”

Section: Introductionmentioning

confidence: 99%

Differential tissue growth and patterns of cell death in mouse limb autopod morphogenesis

Salas‐Vidal

Valencia

Covarrubias

2001

Developmental Dynamics

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Programmed cell death (PCD) is considered one of the most important cellular processes in the morphogenesis of organs and tissues during animal development. Although the embryonic limb has been established as a classic model for the study of PCD, detailed studies on this process' contribution to morphogenesis are still lacking. In the present work, using modern computer-aided techniques, we estimated the contribution of PCD to mouse limb morphogenesis. For the detection of apoptotic cell death, we stained whole embryonic limbs with acridine orange or, in some instances, used the TUNEL technique, and visualized the tissues by confocal laser scanning microscopy. We found that cell death patterns are dynamic during limb development, and occur in gradients oriented with the main limb axes, anteroposterior, dorsoventral and distoproximal. Interdigital apoptosis in the autopod was initially detected at the most distal region, and then more proximally as development proceeded. Interestingly, we found that digit separation is more pronounced on the dorsal side, contrary to what is expected from the apoptotic cell distribution, which shows more abundant cell death in the ventral region. Using 2-D and 3-D models, we found that most digit individualization occurs rather by digit growth than by interdigital cell death. Therefore, digits do not mainly individualize by degeneration of preformed interdigital tissue, but probably by a dynamic balance between proliferation and cell death, reducing interdigital growth, which results in protrusion of digits. We determined the expression pattern of fgf-8 during the period of digit individualization, as the product of this gene could participate in defining the limb growth pattern. Initially, fgf-8 expression was coincident with the apical ectodermal ridge, but when cell death was first detected in the interdigits, fgf-8 expression became restricted to the tip of the growing digits. Therefore, FGF-8 could be one of the factors responsible for differential digit-interdigit growth, and might also act as a survival factor on interdigital tissue. We also found that the expression patterns of rar-␤, bmp-2, bmp-4, bmp-7, msx-1, and msx-2 genes, proposed to be involved in the activation of interdigital cell death, did not overlap with, or were not highly expressed in the major zones of cell death in the developing limb.

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Developmental cell death: morphological diversity and multiple mechanisms

Cited by 1,536 publications

References 125 publications

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

Differences in DNA Fragmentation following Transient Cerebral or Decapitation Ischemia in Rats

Chronic UVA irradiation of human HaCaT keratinocytes induces malignant transformation associated with acquired apoptotic resistance

Differential tissue growth and patterns of cell death in mouse limb autopod morphogenesis

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