Techniques for demonstrating cell death

Bowen, I. D.

doi:10.1007/978-94-011-6921-9_14

Cited by 51 publications

(51 citation statements)

References 166 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The presence of hydrolases has been described before for apoptotic cells in general (Bowen, 1981). Peroxidase activity in apoptotic cells was found earlier in our studies on carp skin (Iger, 1992;Y.…”

Section: Epidermissupporting

confidence: 84%

Cellular responses in the skin of the trout (Oncorhynchus mykiss) exposed to temperature elevation

Iger

Jenner

Bonga

1994

Journal of Fish Biology

View full text Add to dashboard Cite

The skin of rainbow trout was examined at the ultrastructural and cytochemical level after a 3-h exposure to an elevation of the water temperature, from 15 to 22° C. Within 3 h, the thickness of the epidermis had significantly (P <0 05) decreased when compared to control fish. After 24 h it was restored, and from day 4 onwards even increased above control levels. The thickening of the epidermis was associated with appearance of many mitotic cells, not observed in control fish. Within 24 h many apoptotic epidermal cells were found, indicating enhanced ageing of the cells. Filament cells from the outer epidermal layers synthesized vesicles with peroxidase activity within 3 h after temperature elevation. This enzyme was found also in apoptotic as well as in necrotic filament cells. Mucous cells became elongated and their mucosomes displayed peroxidase activity. Occasionally electrondense, probably serous, mucosomes appeared. In the epidermis rodlet cells were found. Both epideimis and dermis, became invaded by many lymphocytes and macrophages. The latter contained vesicles with peroxidase activity. Pigment-containing cytoplasmic extensions of melanocytes penetrated the epidermis while iridocyles disappeared from the dermis. The synthetic activity of dermal fibroblasts was stimulated. These results show that a moderate temperature elevation has pronounced and prolonged effects on the skin of the exposed fish. The effects are to a high extent comparable with those of stressors such as heavy metals, acid water or wounding.

show abstract

Section: Epidermissupporting

confidence: 84%

Cellular responses in the skin of the trout (Oncorhynchus mykiss) exposed to temperature elevation

Iger

Jenner

Bonga

1994

Journal of Fish Biology

View full text Add to dashboard Cite

show abstract

“…This indi cates that cell death in the branchial epithelium is mostly physiologically controlled, and only indirectly influenced by external factors (Wyllie et al 1980;Bowen 1981). Acci dental cell death, structurally reflected by necrosis, is mainly observed immediately after abrupt freshwater to seawater transfer, but rarely in fully adapted freshwater or seawater O. mosscunbicus.…”

Section: Differentiation and Degenerationmentioning

confidence: 99%

“…In contrast to the latter, they are physiological in nature and include hor mones, other humoral substances and tissue factors. Intrin sic cell death or apoptosis has become recognised as a physi ological mechanism that is part of the genetic program con trolling the balance between cell division, differentiation and deletion in many epithelia and other tissues (Wyllie 1981 ;Bowen 1981). Extrinsic factors may induce apoptosis indirectly, e.g.…”

mentioning

confidence: 99%

Degeneration and death, by apoptosis and necrosis, of the pavement and chloride cells in the gills of the teleost Oreochromis mossambicus

1989

View full text Add to dashboard Cite

Summary. Degeneration and death of branchial epithelial cells were studied in an African cichlid fish. In both fresh water and seawater fish the superficially located pavement cells are sloughed off at the end of their lifecycle. This process is preceded by degeneration via a process of cyto plasmic shrinkage and condensation related to apoptotic (physiologically controlled) cell death. The chloride cells are pleomorphic, i.e., accessory, mature, and degenerating cells. Degeneration of chloride cells mainly occurs by apop tosis. Degenerating cells show shrinkage and densification of cytoplasm and nuclei, and swelling of the tubular system; these cells are then separated from the ambient water by pavement cells. They are finally phagocytosed and digested by macrophages. Apoptosis of chloride cells, but not of pavement cells, is greatly stimulated when the fish are in seawater; this reflects an increase in cellular turnover of the chloride cells. Accidental cell death (necrosis) of pave ment cells or chloride cells is rarely observed in fully adapted freshwater and seawater fish. Its incidence in creases in the first few days following transfer of fish from fresh water to seawater.

show abstract

“…8 No proteases have been clearly implicated in the necrotic degradation of PARP-1, however it has been shown that during the course of necrosis, the content of lysosomes is released into the cytosol. 9 This event might allow the proteases liberated to access to cytosolic and nuclear proteins like PARP-1 and process them.…”

Section: Introductionmentioning

confidence: 99%

Characterization of the necrotic cleavage of poly(ADP-ribose) polymerase (PARP-1): implication of lysosomal proteases

et al. 2001

View full text Add to dashboard Cite

The poly(ADP-ribose) polymerase (PARP-1), a 113 kDa nuclear enzyme, is cleaved in fragments of 89 and 24 kDa during apoptosis. This cleavage has become a useful hallmark of apoptosis and has been shown to be done by DEVD-ase caspases, a family of proteases activated during apoptosis. Interestingly, PARP-1 is also processed during necrosis but a major fragment of 50 kDa is observed. This event is not inhibited by zVAD-fmk, a broad spectrum caspase inhibitor, suggesting that these proteases are not implicated in the necrotic cleavage of PARP-1. Since lysosomes release their content into the cytosol during necrosis, the proteases liberated could produce the cleavage of PARP-1. We therefore isolated lysosomal rich-fractions from Jurkat T cells. Our results reveal that the in vitro lysosomal proteolytic cleavage of affinity purified bovine PARP-1 is composed of fragments corresponding, in apparent molecular weight and function, to those found in Jurkat T cells treated with necrotic inducers like 0.1% H 2 O 2 , 10% EtOH or 100 mM HgCl 2 . Moreover, we used purified lysosomal proteases (cathepsins B, D and G) in an in vitro cleavage assay and found that cathepsins B and G cleaved PARP-1 in fragments also found with the lysosomal rich-fractions. These findings suggest that the necrotic cleavage of PARP-1 is caused in part or in totality by lysosomal proteases released during necrosis. Cell Death and Differentiation (2001) 8, 588 ± 594.

show abstract

Techniques for demonstrating cell death

Cited by 51 publications

References 166 publications

Cellular responses in the skin of the trout (Oncorhynchus mykiss) exposed to temperature elevation

Cellular responses in the skin of the trout (Oncorhynchus mykiss) exposed to temperature elevation

Degeneration and death, by apoptosis and necrosis, of the pavement and chloride cells in the gills of the teleost Oreochromis mossambicus

Characterization of the necrotic cleavage of poly(ADP-ribose) polymerase (PARP-1): implication of lysosomal proteases

Contact Info

Product

Resources

About