Apoptosis induced by cold shock in vitro is dependent on cell growth phase

Soloff, Bernard L.; Nagle, William A.; Moss, A. J.; Henle, Kurt J.; Crawford, Jack T.

doi:10.1016/0006-291x(87)91046-1

Cited by 65 publications

(38 citation statements)

References 17 publications

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“…Our data proved that p38-MAPK activity was not responsible for LLC-PK1 cold-induced cell death although transplant animal models have confirmed an improvement of heart, lung or liver functions after preservation in the presence of an inhibitor of p38-MAPK (6,8,34). In fact, abundant evidence for p38-MAPK involvement in apoptosis, especially at rewarming step, exists (33,35); however, we show here that apoptosis did not occur in our model. Quite surprisingly, PEG35 elicited upregulations of JNK phosphorylation and activity in both cold-preservation models.…”

Section: Discussioncontrasting

confidence: 48%

Protective Effect of PEG 35 000 Da on Renal Cells: Paradoxical Activation of JNK Signaling Pathway During Cold Storage

Dutheil

Rioja-Pastor

Tallineau

et al. 2006

American Journal of Transplantation

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Polyethylene glycol (PEG), a high-molecular weight colloid, is added to preservation solutions in order to decrease cold-and ischemia-induced injuries of the grafted organ. We evaluated on LLC-PK1, a porcine proximal tubular epithelial cell line (1) the efficiency of several commercial preservation solutions (University of Wisconsin, Euro-Collins, Celsior, SCOT, IGL-1), and (2) whether adding PEG (400-35 000 Da) in a simple extracellular-type buffer modified cell integrity and mitogen-activated protein kinase (MAPK) signaling pathways. SCOT was the most efficient commercial solution. Moreover, only PEG 35 000 Da totally preserved cell viability, induced a decrease on reactive oxygen species production and a decrease on p38-MAPK activation. Furthermore PEG 35 000 Da stimulated c-Jun N-terminal kinase (JNK). However, the inhibition of JNK pathway, with the specific SP600125 inhibitor, in the presence of PEG 35 000 Da did not affect cell survival. We also confirmed on whole pig kidney the protective effect of PEG 35 000 Da on cold-induced tubular injuries. This study confirms PEG antioxidative properties, but we demonstrate that its effect on JNK signaling pathway had also a paradoxical effect on cell death. This sheds a new light on PEG effects during cell preservation, independently from the classical immuno-camouflaging hypothesis.

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Section: Discussioncontrasting

confidence: 48%

Protective Effect of PEG 35 000 Da on Renal Cells: Paradoxical Activation of JNK Signaling Pathway During Cold Storage

Dutheil

Rioja-Pastor

Tallineau

et al. 2006

American Journal of Transplantation

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“…This term also includes cell deaths that may not exhibit some of the typical features of apoptosis, such as DNA degradation. There (51,(61)(62)(63).…”

mentioning

confidence: 99%

Toward an understanding of the molecular mechanisms of physiological cell death.

Vaux

1993

Proc. Natl. Acad. Sci. U.S.A.

542

242

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Cell death is a normal physiological process. Morphological studies have shown that cells that die by physiological mechanisms often undergo characteristic changes termed "apoptosis" or "programmed cell death." Recent work has begun to unravel the molecular mechanisms of these deaths and has shown that one of the primary cell-death pathways is conserved throughout much of evolution. In the nematode Caenorhabditis elegans programmed cell deaths are mediated by a mechanism controlled by the ced-9 gene; in mammals apoptosis can often be inhibited by expression of the bcl-2 gene. The ability of the human BCL2 gene to prevent cell deaths in C. elegans strongly suggests that bcl-2 and ced-9 are homologous genes. Although the process of cell death controlled by bcl-2 can occur in many cell types, there appears to be more than one physiological cell-death mechanism. Targets of cytotoxic T cells and cells deprived of growth factor both exhibit changes characteristic of apoptosis, such as DNA degradation. However, bcl-2 expression protects cells from factor withdrawal but fails to prevent cytotoxic T-cell killing. DNA degradation is, thus, not specific for any one cell-death mechanism. The ability of bcl-2 to protect cells from a wide variety of pathological, as well as physiological, stimuli indicates that many triggers can serve to activate the same suicide pathway, even some thought to cause necrosis, and not physiological cell death.

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“…In contrast to our study, Blanco-Rodriguez et al, in 1997 indicated an increase in spermatogonial apoptosis during stages XII and XIV following testicular local hypothermia at 10ºC (16). In vitro studies on hamster fibroblast cells (31) and human synovial cells have also shown a relationship between cold shock-induced apoptosis and the cell cycle (32). These contraries may be due to the nature (in vivo or in vitro) and design of the study, for instance we forced our mice to swim in water while in Blanco's study the animal's bodies were out of water.…”

Section: Discussionmentioning

confidence: 99%

Spermatogenesis Process Following Chronic Swimming and Standing in Cold, Warm and Lukewarm Water

2014

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Background: Physical activity and alteration of temperature as a source of stress may have adverse effects on male reproduction. Objectives: The aim of this study was to investigate the effect of chronic swimming and standing in cold, warm and lukewarm water on mouse spermatogenesis. Materials and Methods: Forty-nine male mice (N = 49) were randomly divided into seven groups: C, control; SwC, swimming in cold water (10°C); StC, standing in cold water (10°C); SwL, swimming in lukewarm water (23°C); StL, standing in lukewarm water (23°C); SwW, swimming in warm water (36°C); StW, standing in warm water (36°C). Animals in swimming groups were submitted to daily forced swimming for five minutes for five consecutive days/week during five weeks. However groups StC, StL and StW were only standing on a raised platform inside the water pool, without swimming, for the same time and duration. Evaluations on day 36 were made using enzyme linked immunosorbent assay (ELISA), Johnsen score and immunohistochemistry for assay of serum testosterone, luteinizing hormone (LH) levels, quality of spermatogenesis and detection of apoptosis, respectively. Results: Serum LH and testosterone levels as well as Johnsen score were significantly reduced in all groups except for the group standing in lukewarm water (P < 0.05). Apoptosis was increased only in the swimming or standing in warm water groups (P < 0.05). Conclusions: This study indicates that forced swimming and standing in all water temperatures has adverse effects on male fertility parameters, the only exception is standing in lukewarm water, which seems to be safe for male fertility parameters.

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Apoptosis induced by cold shock in vitro is dependent on cell growth phase

Cited by 65 publications

References 17 publications

Protective Effect of PEG 35 000 Da on Renal Cells: Paradoxical Activation of JNK Signaling Pathway During Cold Storage

Protective Effect of PEG 35 000 Da on Renal Cells: Paradoxical Activation of JNK Signaling Pathway During Cold Storage

Toward an understanding of the molecular mechanisms of physiological cell death.

Spermatogenesis Process Following Chronic Swimming and Standing in Cold, Warm and Lukewarm Water

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