Necrotic volume increase and the early physiology of necrosis

Barros, L. Felipe; Hermosilla, Tamara; Castro, Joel

doi:10.1016/s1095-6433(01)00438-x

Cited by 129 publications

(105 citation statements)

References 55 publications

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“…Tissue and cell type specificity, and the extent or nature of injury and death signals should all be taken into consideration (Barros et al 2001;Rosser and Gores 1995;Strauss and Morton 2003). It was found that after anoxia or 5-12 mM NaCN exposure, PC12 cells or NGF-induced differentiated PC12 cells were equally injured leading to death by necrosis.…”

Section: Discussionmentioning

confidence: 99%

The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells

Wu¹,

Ma²,

Fan³

et al. 2010

Cell Stress and Chaperones

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It has been demonstrated that hypoxic preconditioning (HP) enhances the survival ability of the organism against the subsequent acute anoxia (AA). However, it is not yet clear whether necrosis induced by AA can be prevented by HP, and what are the underlying mechanisms. In this study, we examined the effect of HP (10% O 2 , 48 h) on necrosis induced by AA (0% O 2 , 24 h) in PC12 cells. We found that HP delayed the regulatory volume decrease and reduced cell swelling after 24 h of exposure to AA. Since aldose reductase (AR) is involved in cell volume regulation, we detected AR mRNA expression with reverse transcription-polymerase chain reaction (RT-PCR) techniques. The AR mRNA level was dramatically elevated by HP. Furthermore, an HP-induced decrease in cell injury was reversed by berberine chloride (BB), the inhibitor of AR. In addition, sorbitol synthesized from glucose catalyzed by AR is directly related to cell volume regulation. Subsequently, we tested sorbitol content in the cytoplasm. HP clearly elevated sorbitol content, while BB inhibited the elevation induced by HP. Further study showed that a strong inhibitor of sorbitol permease, quinidine, completely reversed the protection induced by HP after AA. These data provide evidence that HP prevents necrosis induced by AA and is mediated by AR and sorbitol pathway.

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Section: Discussionmentioning

confidence: 99%

The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells

Wu¹,

Ma²,

Fan³

et al. 2010

Cell Stress and Chaperones

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“…The factors contributing to necrosis are mostly extrinsic in nature, such as osmotic, thermal, toxic, hypoxic-ischemic, and traumatic insults (25,60). Necrosis is characterized by progressive loss of cytoplasmic membrane integrity, rapid influx of Na ϩ , Ca 2ϩ , and water, resulting in cytoplasmic swelling and nuclear pyknosis (9,18,200,244). The latter feature leads to cellular fragmentation and release of lysosomal and granular contents into the surrounding extracellular space, with subsequent inflammation (138).…”

Section: Modes Of Cell Deathmentioning

confidence: 99%

“…The same type of insult can induce either apoptosis or necrosis, but whether one mode of cell death is preferred over the other usually depends on the severity of the insult and the idiosyncrasy of the target cell (9,25,128,141). The perception that apoptosis and necrosis are functionally opposed forms of cell death is fading, and a consensus has developed that both forms of cell death constitute two extremes of a continuum.…”

Section: Modes Of Cell Deathmentioning

confidence: 99%

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

Padanilam

2003

American Journal of Physiology-Renal Physiology

334

268

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In humans and experimental models of renal ischemia, tubular cells in various nephron segments undergo necrotic and/or apoptotic cell death. Various factors, including nucleotide depletion, electrolyte imbalance, reactive oxygen species, endonucleases, disruption of mitochondrial integrity, and activation of various components of the apoptotic machinery, have been implicated in renal cell vulnerability. Several approaches to limit the injury and augment the regeneration process, including nucleotide repletion, administration of growth factors, reactive oxygen species scavengers, and inhibition of inducers and executioners of cell death, proved to be effective in animal models. Nevertheless, an effective approach to limit or prevent ischemic renal injury in humans remains elusive, primarily because of an incomplete understanding of the mechanisms of cellular injury. Elucidation of cell death pathways in animal models in the setting of renal injury and extrapolation of the findings to humans will aid in the design of potential therapeutic strategies. This review evaluates our understanding of the molecular signaling events in apoptotic and necrotic cell death and the contribution of various molecular components of these pathways to renal injury.

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“…Although an increase in oocyte and follicular diameter after 28 days of culture with FSH-2d was demonstrated, our TEM findings suggest that this light microscopically observed phenomenon is due to follicular necrosis, characterized by cell swelling as a result of increased cellular vacuolization (Barros et al, 2001). As there are FSH receptors in the granulosa cells of early follicles, it is possible that FSH may promote follicular growth and development (Méduri et al, 2002).…”

Section: Discussionmentioning

confidence: 59%

In vitro development of primordial follicles after long-term culture of goat ovarian tissue

Matos

Bruno

Rocha

et al. 2011

Research in Veterinary Science

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This study aims to investigate the effects of follicle stimulating hormone (FSH) and fibroblast growth factor-2 (FGF-2) on the survival and growth of caprine preantral follicles. Ovarian tissues were cultured for 1, 7, 14, 21 or 28 days in medium supplemented with FSH (FSH-2d or FSH-7d, i.e., with replacement of the culture medium every 2 or 7 days, respectively) or FSH + FGF-2 (replacement of the medium every 2 days). Non-cultured (control) and cultured ovarian fragments were processed for histological and ultrastructural analysis. After 28 days of culture, the media supplemented with FSH-2d was the most effective in maintaining the percentage of normal follicles and in promoting follicular growth. Furthermore, both treatments with FSH increased the percentage of the primary follicles. However, ultrastructural studies did not confirm follicular integrity from 14 days of culture onward. In conclusion, culturing tissue for up to 7 days in medium containing FSH alone or combined with FGF-2 maintains caprine preantral follicle integrity and promotes their growth in vitro.

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Necrotic volume increase and the early physiology of necrosis

Cited by 129 publications

References 55 publications

The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells

The anti-necrosis role of hypoxic preconditioning after acute anoxia is mediated by aldose reductase and sorbitol pathway in PC12 cells

Cell death induced by acute renal injury: a perspective on the contributions of apoptosis and necrosis

In vitro development of primordial follicles after long-term culture of goat ovarian tissue

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