Apoptosis detection: an overview

Sgonc, Roswitha; Gruber, Johann

doi:10.1016/s0531-5565(98)00031-x

Cited by 131 publications

(97 citation statements)

References 32 publications

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“…To address whether apoptosis of HeLa cells is induced in the presence of TC, we treated exponentially growing HeLa cells with 15ng/ml TC for 24 h. An apoptotic population was identified from the TC-treated cells as measured by Annexin-V [35,36] or M30 assay [37,38] (Fig. 2A, 2B).…”

Section: P53 Dependence Of Tc-induced Apoptosis Of Hela Cellsmentioning

confidence: 99%

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

et al. 2005

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Recent studies indicate that cell-cycle checkpoints are tightly correlated with the regulation of apoptosis, in which p53 plays an important role. Our present works show that the expression of E6/E7 oncogenes of human papillomavirus in HeLa cells is inhibited in the presence of anti-tumor reagent tripchlorolide (TC), which results in the up-regulation of p53 in HeLa cells. Interestingly, under the same TC-treatment, the cells at the early S-phase are more susceptible to apoptosis than those at the middle S-phase although p53 protein is stabilized to the same level in both situations. Significant difference is exhibited between the two specified expression profiles. Further analysis demonstrates that anti-apoptotic gene survivin is up-regulated by p53 in the TC-treated middle-S cells, whereas it is down-regulated by p53 in the TC-treated early-S cells. Taken together, the present study indicates that the differential p53-regulated expression of survivin at different stages of the cell cycle results in different cellular outputs under the same apoptosis-inducer.

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Section: P53 Dependence Of Tc-induced Apoptosis Of Hela Cellsmentioning

confidence: 99%

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

et al. 2005

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“…Since the first definition of apoptosis in 1972 [46], a wide array of methods have been developed for detection of apoptosis (Table 3) [47]. Apoptosis was initially a morphological diagnosis [46], and transmission electron microscopy still appears to be the gold standard [47].…”

Section: Apoptotic Cell Death During In Vitro Culturementioning

confidence: 99%

New Strategies in the Treatment of Acute Myelogenous Leukemia (AML): In Vitro Culture of AML Cells—The Present Use in Experimental Studies and the Possible Importance for Future Therapeutic Approaches

et al. 2001

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In vitro studies of cultured native acute myelogenous leukemia (AML) blasts and cell lines have contributed significantly to our present knowledge about the pathogenesis of AML. In the present article we review different techniques for preparation and in vitro culture of AML blasts. Well-characterized serum-free in vitro conditions can now be used in experimental studies of AML, and this makes comparisons between different studies easier. We also describe assays for characterization of AML progenitor subsets (i.e., suspension cultures, colony assays, long-term in vitro culture, xenotransplantation in immunocompromised mice), and we discuss the possible use of AML cell lines as experimental models in AML. Furthermore, clinical studies suggest that the in vitro growth characteristics of AML blasts assayed by short-term culture of the total native populations can be used as a predictor of prognosis after intensive chemotherapy. These in vitro assays may therefore be used for more accurate identification of prognostic parameters and thereby form a basis for the development of simplified laboratory techniques suitable for routine evaluation of patients undergoing risk-adapted therapy. However, it will be equally important to further evaluate the clinical relevance of assays for primitive AML progenitors, and to develop simplified methods that can be used to characterize these progenitor subsets in the routine clinical evaluation.

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“…Artifacts inherent in techniques that detect double-stranded DNA breaks as well as overlaps between apoptotic and necrotic death programs account for these problems (59,60). Current assays are limited in their capacities to distinguish between apoptosis and necrosis in myocytes.…”

Section: Myocardial Necrosismentioning

confidence: 99%

Molecular and cellular mechanisms of cardiotoxicity.

Kang

2001

Environ Health Perspect

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Cardiotoxicity resulting from detrimental environmental insults has been recognized for a long time. However, extensive studies of the mechanisms involved had not been undertaken until recent years. Advances in molecular biology provide powerful tools and make such studies possible. We are gathering information about cellular events, signaling pathways, and molecular mechanisms of myocardial toxicologic responses to environmental toxicants and pollutants. Severe acute toxic insults cause cardiac cell death instantly. In the early response to mild environmental stimuli, biochemical changes such as alterations in calcium homeostasis occur. These may lead to cardiac arrhythmia, which most often is reversible. Prolonged stimuli activate transcription factors such as activator protein-1 through elevation of intracellular calcium and the subsequent activation of calcineurin. Upregulation by activated transcription factors of hypertrophic genes results in heart hypertrophy, which is a short-term adaptive response to detrimental factors. However, further development of hypertrophy will lead to severe and irreversible cardiomyopathy, and eventually heart failure. From cardiac hypertrophy to heart failure, myocardial cells undergo extensive biochemical and molecular changes. Cardiac hypertrophy causes tissue hypoperfusion, which activates compensatory mechanisms such as production of angiotensin II and norepinephrine. Both further stimulate cardiac hypertrophy and, importantly, activate counterregulatory mechanisms including overexpression of atrial natriuretic peptide and b-type natriuretic peptide, and production of cytokines such as tumor necrosis factor-alpha. This counterregulation leads to myocardial remodeling as well as cell death through apoptosis and necrosis. Cell death through activation of mitochondrial factors and other pathways constitutes an important cellular mechanism of heart failure. Our current knowledge of cardiotoxicity is limited. Further extensive studies are warranted for a comprehensive understanding of this field.

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Apoptosis detection: an overview

Cited by 131 publications

References 32 publications

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

Differential regulation of survivin by p53 contributes to cell cycle dependent apoptosis

New Strategies in the Treatment of Acute Myelogenous Leukemia (AML): In Vitro Culture of AML Cells—The Present Use in Experimental Studies and the Possible Importance for Future Therapeutic Approaches

Molecular and cellular mechanisms of cardiotoxicity.

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