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  • Articles  (30)
  • Apoptosis  (30)
  • Springer  (30)
  • Cambridge University Press
  • Nature Publishing Group
  • Periodicals Archive Online (PAO)
  • Springer Nature
  • Taylor & Francis
  • 2020-2024
  • 2005-2009
  • 2000-2004  (30)
  • 1965-1969
  • 1945-1949
  • 2003
  • 2000  (30)
  • 1965
  • Biology  (30)
  • Philosophy
  • Economics
  • Process Engineering, Biotechnology, Nutrition Technology
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  • Articles  (30)
Source
Keywords
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Years
  • 2020-2024
  • 2005-2009
  • 2000-2004  (30)
  • 1965-1969
  • 1945-1949
Year
  • 2003
  • 2000  (30)
  • 1965
Topic
  • 1
    Electronic Resource
    Electronic Resource
    Identification of okadaic-acid-induced genes by mRNA differential display in glioma cells (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 152-159 
    Details
    ISSN: 1423-0127
    Keywords: Apoptosis ; Differential display ; Glioma ; Okadaic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract To identify novel genes associated with apoptosis in glioma cells, we treated T98G glioma cells with okadaic acid (OA). Differential display using 15 random primers was performed on RNA extracted from these cells. Upregulated bands were excised from polyacrylamide gels and cloned. Northern blots were used to confirm RNA expression in T98G cells. 18 RNA fragments corresponding to the untranslated region of genes were identified and sequenced. Three unknown gene fragments were used to screen a fetal brain cDNA library resulting in three complete cDNA sequences. The three sequences corresponded to a human gene homologous to the yeast translation initiation factor Sui-1, a cAMP-regulated phosphoprotein, ARPP-16/19, and a novel gene designated O48. Transcription of Sui-1 increased in response to all stress factors tested, whereas ARPP only responded to OA. 2-kb and 4-kb O48 RNA species were identified. OA and stress factors increased 2-kb expression while K252a (protein kinase inhibitor) increased 4-kb expression. Differential display is effective for identifying genes associated with apoptosis. Novel genes may be identified by further analysis of the gene fragments identified in this study. The function of O48 is unknown.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02256622
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  • 2
    Electronic Resource
    Electronic Resource
    Delta opioid peptide [D-Ala2,D-Leu5]enkephalin promotes cell survival (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 195-199 
    Details
    ISSN: 1423-0127
    Keywords: Opioid ; Enkephalin ; DADLE ; Transplantation ; Hibernation ; Apoptosis ; Methamphetamine ; Dopamine ; Ischemia ; Reperfusion ; PC12 cells ; Neuroprotection
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract By studying the hibernation in ground squirrels, a protein factor termed hibernation induction trigger (HIT) was found to induce hibernation in summer-active ground squirrels. Further purification of HIT yielded an 88-kD peptide that is enriched in winter hibernator. Partial sequence of the 88-kD protein indicates that it may be related to the inhibitor of metalloproteinase. Delta opioid [D-Ala2,D-Leu5]enkephalin (DADLE) also induced hibernation. HIT and DADLE were found to prolong survival of peripheral organs preserved en bloc or as a single preparation. These organs include the lung, the heart, liver and kidney. DADLE also promotes survival of neurons in the central nervous system. Methamphetamine (METH) is known to cause destruction of dopaminergic (DA) terminals in the brain. DADLE blocked and reversed the DA terminal damage induced by METH. DADLE acted against this effect of METH at least in part by attenuating the mRNA expressions of a tumor necrosis factor p53 and an immediate early gene c-fos. DADLE also blocked the neuronal damage induced by ischemia-reperfusion following a transient middle cerebral artery occlusion. In PC12 cells, DADLE blocked the cell death caused by serum deprivation in a naltrexone-sensitive manner. Thus, DADLE, and by extension the endogenous delta opioid peptides and delta opioid receptors, may play an important role in organ and neuronal survival. Here, critical developments concerning these fascinating cell protective properties of DADLE are reviewed.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02255466
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  • 3
    Electronic Resource
    Electronic Resource
    Differential apoptosis effects of primate lentiviral Vpr and Vpx in mammalian cells (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 322-333 
    Details
    ISSN: 1423-0127
    Keywords: Apoptosis ; HIV ; SIV ; Vpr ; Vpx ; Bcl-2 ; Bax
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract The growth inhibitory effects of Vpr and Vpx are species-and cell type-dependent. HIV-1, HIV-2 and SIV Vpr are primarily cytostatic in mammalian cells and HIV-1 Vpr has been reported to induce apoptosis in human cells. Our previous studies have shown that HIV-1, HIV-2 and SIV Vpr and Vpx have differential cytostatic and cytotoxic effects in the yeast cells [Zhang et al.: Virology, 230:103–112; 1997]. Here, we further examined the apoptosis function of HIV-1 Vpr in different species of mammalian cells and investigated if other primate lentiviral Vpr and Vpx exert similar functions. Our results show that none of the primate lentiviral Vpr or Vpx we tested induces apoptosis in nonhuman species of mammalian cells. However, HIV-1 Vpr, but not HIV-2 or SIV Vpr and/or Vpx, induced apoptosis in different types of human cell lines. Further, the apoptotic effect of HIV-1 Vpr can be distinguished from that of the human interferon-γ, a known proapoptotic protein, that HIV-1 Vpr shows little to no paracrine and/or bystander effect. When coexpressed with Bcl-2 or Bcl-XL, the apoptotic effect of HIV-1 Vpr became markedly attenuated. These results indicate that the apoptotic effect of HIV-1 Vpr is species-dependent and is intracellularly modulated by the Bcl-2 family of proteins. Our study also suggests that the proapoptotic function of HIV-1 Vpr is developmentally associated with human but not nonhuman primate species.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253252
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  • 4
    Electronic Resource
    Electronic Resource
    Apoptosis occurs in a new model of thermal brain injury (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 459-465 
    Details
    ISSN: 1423-0127
    Keywords: Apoptosis ; Thermal brain injury
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Apoptosis has been implicated recently as a prominent response of the brain to a variety of insults, such as ischemia and trauma. In this study, we demonstrate that apoptosis is a prominent part of the brain's response to a thermal insult. To examine the brain's response to a thermal insult, a new model of thermal brain injury in the laboratory rat was developed. Water heated to 60°C was passed over an area of thinned calvarium for 1 min. This resulted in an actual brain temperature of 47–48°C. A uniform area of 2,3,5-triphenyl-tetrazolium chloride pallor was demonstrated and pyknotic neurons were seen in the area of injury by hematoxylin-eosin staining. Apoptosis was demonstrated by the characteristic DNA fragmentation seen by agarose gel electrophoresis, ApopTag in situ staining and electron microscopy. The findings of apoptosis were localized to the area of thermal injury and were time dependent, starting 6 h after the insult and peaking approximately 18 h after the insult. This represents one of the first demonstrations that apoptosis occurs in the brain in response to a thermal injury.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02253361
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  • 5
    Electronic Resource
    Electronic Resource
    Mitochondrial role in life and death of the cell (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 2-15 
    Details
    ISSN: 1423-0127
    Keywords: Apoptosis ; Mitochondria ; Necrosis ; Oxidative stress ; Reactive oxygen species
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Mitochondria are the major ATP producer of the mammalian cell. Moreover, mitochondria are also the main intracellular source and target of reactive oxygen species (ROS) that are continually generated as by-products of aerobic metabolism in human cells. A low level of ROS generated from the respiratory chain was recently proposed to take part in the signaling from mitochondria to the nucleus. Several structural characteristics of mitochondria and the mitochondrial genome enable them to sense and respond to extracellular and intracellular signals or stresses in order to sustain the life of the cell. It has been established that mitochondrial respiratory function declines with age, and that defects in the respiratory chain increase the production of ROS and free radicals in mitochondria. Within a certain concentration range, ROS may induce stress responses of the cell by altering the expression of a number of genes in order to uphold energy metabolism to rescue the cell. However, beyond this threshold, ROS may elicit apoptosis by induction of mitochondrial membrane permeability transition and release of cytochrome c. Intensive research in the past few years has established that mitochondria play a pivotal role in the early phase of apoptosis in mammalian cells. In this article, the role of mitochondria in the determination of life and death of the cell is reviewed on the basis of recent findings gathered from this and other laboratories.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02255913
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  • 6
    Electronic Resource
    Electronic Resource
    p53 gene status modulates the chemosensitivity of non-small cell lung cancer cells (2000)
    Springer
    Journal of biomedical science 7 (2000), S. 64-70 
    Details
    ISSN: 1423-0127
    Keywords: p53 ; Chemosensitivity ; Cell cycle ; Apoptosis ; Non-small cell lung cancer
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract This study examined the effects of p53 gene status on DNA damage-induced cell death and chemosensitivity to various chemotherapeutic agents in non-small cell lung cancer (NSCLC) cells. A mutant p53 gene was introduced into cells carrying the wild-type p53 gene and also vice versa to introduce the wild-type p53 gene into cells carrying the mutant p53 gene. Chemosensitivity and DNA damage-induced apoptosis in these cells were then examined. This study included five cell lines, NCI-H1437, NCI-H727, NCI-H441 and NCI-H1299 which carry a mutant p53 gene and NCI-H460 which carries a wild-type p53 gene. Mutant p53-carrying cells were transfected with the wild-type p53 gene, while mutant p53 genes were introduced into NCI-H460 cells. These p53 genes were individually mutated at amino acid residues 143, 175, 248 and 273. The representative cell line NCI-H1437 cells transfected with wild-type p53 gene (H1437/wtp53) showed a dramatic increase in susceptibility to three anticancer agents (7-fold to cisplatin, 21-fold to etoposide, and 20-fold to camptothecin) compared to untransfected or neotransfected H1437 cells. An increase in chemosensitivity was also observed in wild-type p53 transfectants of H727, H441, H1299 cells. The results of chemosensitivity were consistent with the observations on apoptotic cell death. H1437/wtp53 cells, but not H1437 parental cells, exhibited a characteristic feature of apoptotic cell death that generated oligonucleosomal-sized DNA fragments. In contrast, loss of chemosensitivity and lack of p53-mediated DNA degradation in response to anticancer agents were observed in H460 cells transfected with mutant p53. These observations suggest that the increase in chemosensitivity was attributable to wild-type p53 mediation of the process of apoptosis. In addition, our results also suggest that p53 gene status modulates the extent of chemosensitivity and the induction of apoptosis by different anticancer agents in NSCLC cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02255920
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  • 7
    Electronic Resource
    Electronic Resource
    UV-Induced Apoptosis in Resistant HeLa Cells (2000)
    Springer
    Bioscience reports 20 (2000), S. 99-108 
    Details
    ISSN: 1573-4935
    Keywords: Apoptosis ; DNA repair ; UV-resistance ; HeLa
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Chemistry and Pharmacology
    Notes: Abstract Recently, apoptosis (genetically programmed cell death) induced by UV hasbeen documented in some cell culture models. However, the significance ofapoptosis in UV-induced cytotoxicity and resistance is uncertain. In thisstudy, we investigated the induction of apoptosis in HeLa cells and itsrole in acquired UV-resistance. The membrane receptor Fas was induced toassembly, and its immediate downstream target, caspase-8, was induced byUV in a dose- and time-dependent manner. Caspase-10, another possiblecandidate for forming the death-inducing signaling complex with Fas, wasalso activated in a dose- and time-dependent manner. There was significantactivation of caspase 9, 3 and 2 by UV. The apoptotic pathways appeared tobe normal in acquired UV-resistant HeLa cells. In addition, there was a UVdose-dependent induction of chromatin condensation in both parental andUV-resistant cells. However, resistant cells displayed significant reductionin chromatin condensation at lower doses. Inhibition of caspase-3 activation byspecific inhibitor significantly reduced the chromatin condensation in bothcell types, and unexpectedly, the difference between the two cell lines wascompletely eradicated, suggesting that the caspase-3 pathway plays asignificant role in reducing apoptosis in resistant cells. The resultsindicate that UV induces apoptosis by direct activation of apoptoticproteins in HeLa and resistant cells. Although resistant cells displayedpartial inhibition of UV-induced apoptosis through the caspase-3 pathway,there was no consistent difference in the activation of this and relatedcaspase-9 caspases compared to parental HeLa cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1005515400285
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  • 8
    Electronic Resource
    Electronic Resource
    High-density lipoproteins protect endothelial cells from apoptosis induced by oxidized low-density lipoproteins (2000)
    Springer
    Protoplasma 211 (2000), S. 198-206 
    Details
    ISSN: 1615-6102
    Keywords: Apoptosis ; Atherosclerosis ; Endothelium ; Lipoproteins
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Endothelial lesion by oxidized low-density liproproteins (LDL) is one of the first stages in the development of atherosclerosis. The effect of these lipoproteins can range from a functional lesion of the endothelium to death of the endothelial cells by apoptosis. High-density lipoproteins (HDL) are one of the factors which can have a protective effect against the development of atheromatous plaques. The aim of this study is to establish whether the death of endothelial cells by apoptosis induced by oxidized LDLs is prevented by HDLs. ECV304 endothelial cells and bovine aorta endothelial cells were incubated with native LDLs, oxidized LDLs, and a combination of both oxidized LDLs and HDLs. Oxidized LDLs caused a significant increase of mortality mainly by apoptosis. However, when HDLs were added together with oxidized LDLs the percentage of total mortality, the degree of lipoprotein oxidation in the medium, and the percentage of cells in apoptosis were all significantly decreased. HDLs protect against the cytotoxicity of oxidized LDLs possibly by preventing the propagation of the oxidative chain in these lipoproteins.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01304487
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  • 9
    Electronic Resource
    Electronic Resource
    New functions for coenzyme Q (2000)
    Springer
    Protoplasma 213 (2000), S. 127-133 
    Details
    ISSN: 1615-6102
    Keywords: Mitochondrion ; Oxygen radical ; Antioxidant ; Apoptosis ; Cell growth ; Iron transport
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Coenzyme Q is primarily identified with its role in energy coupling where it is involved in the generation of a proton gradient across membranes to drive ATP formation. Its identification as a significant antioxidant throughout cellular membranes is developing. Its function in other membrane redox systems introduces new functions such as the generation of hydrogen peroxide related to cellular signal systems or the acidification of other organelles. A role in the control of cell growth and apoptosis has also been introduced.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01282150
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  • 10
    Electronic Resource
    Electronic Resource
    Bcl-2 protects against apoptosis-related microtubule alterations in neuronal cells (2000)
    Springer
    Apoptosis 5 (2000), S. 43-51 
    Details
    ISSN: 1573-675X
    Keywords: Apoptosis ; bcl-2 ; microtubules ; neurites ; tau ; taxol.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract Bcl-2 is a gene with clear anti-apoptotic properties in neurodegenerative conditions. One of the earliest hallmarks of degeneration in neuronal cell cultures is the loss of neurite morphology. Therefore the effect of Bcl-2 on neuronal morphology and microtubule stability was studied in nerve growth factor differentiated PC12 cells. Microtubule dynamics were modulated using the microtubule stabilizer taxol and the microtubule destabilizer, okadaic acid, a protein phosphatase inhibitor. It was shown that Bcl-2 protects against both taxol- and okadaic acid induced neurite retraction. Bcl-2 overexpression also significantly reduced the increased ratio of acetylated tubulin over total tubulin induced by taxol treatment. Interestingly, Bcl-2 attenuates the decrease of the same ratio after exposure to okadaic acid, suggesting that Bcl-2 is able to normalize the level of acetylated tubulin. In addition, cell death and nuclear fragmentation, induced by okadaic acid, were reduced in Bcl-2 overexpressing cells. This protection is either downstream or independent of tau phosphorylation as quantitative immunocytochemistry with AT8 showed that Bcl-2 did not modify the level of tau phosphorylation. The data suggest that the protective effect of Bcl-2 on the neuronal cytoskeleton is probably linked to changes in the post-translational modification of tubulin.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1009685609275
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