Apoptosis: the biochemistry and molecular biology of programmed cell death

Schwartzman, R. A.

doi:10.1210/er.14.2.133

Cited by 309 publications

(384 citation statements)

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“…In addition, unlike necrotic death that causes swelling of cells, apoptotic death results in the collapse of the dying cell (Schwartzman and Cidlowski, 1993). Here, we demonstrate that the process of cell death in higher plants may have several characteristics of apoptosis, including degradation of nuclear DNA ( Figure 8) and collapse of cells (Figure 2).…”

Section: Discussionmentioning

confidence: 69%

Coordinated Activation of Programmed Cell Death and Defense Mechanisms in Transgenic Tobacco Plants Expressing a Bacterial Proton Pump.

1995

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In plants, programmed cell death is thought to be activated during the hypersensitive response to certain avirulent pathogens and in the course of severa1 differentiation processes. We describe a transgenic model system that mimics the activation of programmed cell death in higher plants. In this system, expression of a bacterial proton pump in transgenic tobacco plants activates a cell death pathway that may be similar to that triggered by recognition of an incompatible pathogen. Thus, spontaneous lesions that resemble hypersensitive response lesions are formed, multiple defense mechanisms are apparently activated, and systemic resistance is induced in the absence of a pathogen. Interestingly, mutation of a single amino acid in the putative channel of this proton pump rendes it inactive with respect to lesion formation and induction of resistance to pathogen challenge. This transgenic model system may provide insights into the mechanisms involved in mediating cell death in higher plants. In addition, it may also be used as a general agronomic tool to enhance disease protection.

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Section: Discussionmentioning

confidence: 69%

Coordinated Activation of Programmed Cell Death and Defense Mechanisms in Transgenic Tobacco Plants Expressing a Bacterial Proton Pump.

1995

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“…In light of the now well-known association between internucleosomal DNA fragmentation and apoptosis (Williams et al, 1974;Wyllie, 1980;Arends et al, 1990;Schwartzman and Cidlowski, 1993;Tilly, 1994), Zeleznik and co-workers (1989) identified the presence of a cationdependent endonuclease activity in rat ovarian granulosa and luteal cell nuclei capable of eliciting such a pattern of DNA cleavage. Furthermore, the presence of this endonucleolytic activity appeared to be endocrine-regulated, suggesting that the demise of granulosa cells during follicular atresia and of luteal cells during luteolysis, may be dependent upon acquisition of this enzyme during development of the respective tissues.…”

Section: Apoptosis In the Ovary: A Brief Historical Accountmentioning

confidence: 99%

The genes of cell death and cellular susceptibility to apoptosis in the ovary: a hypothesis

Tilly

Perez

1997

Cell Death Differ

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Recent advances in the field of cell death, primarily derived from gene-transfer experiments and manipulation of tumor cell lines in vitro, have identified key genes responsible for determining whether or not a given cell will initiate apoptosis. However, comparatively less is known of the role that the products of these genes play in physiological settings of cell death. In the ovary, a tremendous level of normal cell death takes place in the germline throughout the later stages of fetal development. This process is responsible for setting the absolute number of oocytes (`eggs') available for subsequent development and ovulation during adult life. Interestingly, death remains the fate of the vast majority of oocytes that survive the waves of attrition during fetal life and are endowed in the post-natal ovary as primordial follicles. This pool of oocytes is lost indirectly as a consequence of the death of the somatic (granulosa) cells that, in the case of a small percentage of the total follicles, support and nourish the oocyte until its release at ovulation. Due to the magnitude of cell death that occurs normally within the female gonad during both fetal development and post-natal life, the ovary has proven to be an excellent model to study the role of cell death genes in a physiological setting of endocrine-regulated apoptosis.It is now known that a diverse spectrum of pro-and antiapoptosis susceptibility genes, including members of the bcl-2 and CASP (ced-3/Ice) gene families, are expressed in germ cells and/or somatic cells of the ovary. Many, but not all, of these genes are regulated by specific survival factors, such as gonadotropins and growth factors, and changes in the temporal patterns of cell death gene expression suggest an intimate association exists between the products of these genes and activation of cellular suicide. Moreover, pathological oocyte destruction, such as that triggered by exposure of female germ cells to chemotherapeutic compounds or environmental toxicants, may also be dependent upon genedriven apoptosis. As such, this review will discuss data supporting the hypothesis that the susceptibility of ovarian cells to death induction is dependent upon the pattern of cell death gene expression occurring within those cells prior to and/or concomitant with receipt of the stimulus for apoptosis. Elucidation of the relationship between germ cell loss and cell death genes may allow future intervention into the process of oocyte depletion associated with normal and pathophysiological reproductive senescence.

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“…Apoptosis is involved in the regulation of many intracellular physiological and pathological conditions, including the development of embryos, tissue and organ formation, and immune system generation (Schwartzman and Cidlowski 1993). In mammalian cells, there are two major apoptotic pathways divided into intrinsic mitochondrial and extrinsic death receptor activation (Crow et al 2004;Fischer et al 2004).…”

Section: Introductionmentioning

confidence: 99%

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

Lai

Kuo³

et al. 2014

AGE

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Cardiovascular disease is the second leading cause of death (9.1 %) in Taiwan. Heart function deteriorates with age at a rate of 1 % per year. As society ages, we must study the serious problem of cardiovascular disease. SIRT1 regulates important cellular processes, including anti-apoptosis, neuronal protection, cellular senescence, aging, and longevity. In our previous studies, rats with obesity, high blood pressure, and diabetes exhibiting slowed myocardial performance and induced cell apoptosis were reversed via sports training AGE (2014) 36:9706

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Apoptosis: the biochemistry and molecular biology of programmed cell death

Cited by 309 publications

References 0 publications

Coordinated Activation of Programmed Cell Death and Defense Mechanisms in Transgenic Tobacco Plants Expressing a Bacterial Proton Pump.

Coordinated Activation of Programmed Cell Death and Defense Mechanisms in Transgenic Tobacco Plants Expressing a Bacterial Proton Pump.

The genes of cell death and cellular susceptibility to apoptosis in the ovary: a hypothesis

Exercise training enhanced SIRT1 longevity signaling replaces the IGF1 survival pathway to attenuate aging-induced rat heart apoptosis

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