Mechanism of UV-Induced Apoptosis in Human Leukemia Cells: Roles of Ca2+/Mg2+-Dependent Endonuclease, Caspase-3, and Stress-Activated Protein Kinases

Kimura, Chika; Zhao, Qing‐Li; Kondo, Takashi; Amatsu, Mutsuo; Fujiwara, Yoshisada

doi:10.1006/excr.1997.3912

Cited by 64 publications

(41 citation statements)

References 53 publications

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“…In line with a previous report (19), we found that activation of p38 MAP kinase by UV is not affected by inhibiting caspases-1 and -3 with inhibitors whereas apoptosis was inhibited, as expected. Similarly, we found that activation of NF-kB was also not affected by the same inhibitors.…”

Section: Discussionsupporting

confidence: 93%

“…Takahashi et al suggested a significant role for caspase 1 in UVB-induced apoptosis of SVHK cells (20), but the precise function of caspase-1 in this process is not known. Furthermore, UV triggers apoptosis in human leukemic U937 cells through caspases-1 and -3, and activation of the JNK and p38 MAP kinases is not inhibited by caspase inhibitors, suggesting that neither one of these kinases are important for triggering apoptosis in response to UV in these cells (19). The results from our study suggest that even though UV and IR both trigger apoptosis and HIV gene expression, these pathways are different to some extent since apoptosis and HIV gene expression profiles show different kinetics and magnitude.…”

Section: Discussionmentioning

confidence: 97%

“…Furthermore, death ligands binding to receptors on the cell surface, e.g., members of the (TNF) receptor gene super-family, initiate distinct apoptotic pathways most likely different from those initiated by DNA damage (22,23). The process of apoptosis is concurrent with cell blebbing, activation of caspases that cleave other specific proteins, including PARP, and DNA fragmentation (19,24). Previously, increased HIV gene expression was demonstrated in HeLa cells following exposure to different treatments resulting in cell death, demonstrating dose-dependent HIV gene expression that correlated with the extent of cell death (25).…”

Section: Introductionmentioning

confidence: 99%

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Triggering of Apoptosis is not Sufficient to Induce Human Immunodeficiency Virus Gene Expression

Oakley¹,

Taher²,

Hershey³

et al. 2003

IUBMB Life

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We examined whether there is any causative link between apoptosis and HIV gene expression elicited in response to ultraviolet light (UV) and ionizing radiation (IR). We found that both UV and IR activate HIV gene expression in human T lymphoblastoid 1G5 (HIVluc) cells, but with different kinetics and magnitudes. Treatment with either type of radiation resulted in increased apoptosis, which correlated closely with HIV gene expression. The involvement of caspases in the IR response was demonstrated by using zVAD‐FMK and zDEVD‐FMK caspase inhibitors; both apoptosis and HIV gene expression were inhibited to similar extent. Surprisingly, treatment of 1G5 cells with FAS antibody triggered apoptosis but did not increase HIV gene expression. A correlation between increased apoptosis and gene expression was also demonstrated in human carcinoma HIVcat/A549 cells with UV whereas IR triggered apoptosis but did not activate HIV gene expression. Most significantly, UV activation of HIV gene expression, and NF‐ κB and p38 MAP kinase, both important for efficient HIV gene expression, were not affected by treatment with the zVAD‐FMK and zDEVD‐FMK inhibitors. Treatment of HIVcat/A549 cells with staurosporine or scrape‐loading of cells with cytochrome c resulted in apoptosis but no increase in HIV gene expression. Altogether, a direct correlation exists between apoptosis and HIV gene expression in T‐cells in response to both UV and IR but this is not the case in carcinoma cells. Triggering of apoptosis per se in either cell type does not necessarily result in increased HIV gene expression. Most importantly, the apoptotic and HIV gene expression responses elicited by UV are different to some extent and can be separated. IUBMB Life, 55: 415‐427, 2003

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 97%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Triggering of Apoptosis is not Sufficient to Induce Human Immunodeficiency Virus Gene Expression

Oakley¹,

Taher²,

Hershey³

et al. 2003

IUBMB Life

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“…In murine podocytes, S-100b increases phosphorylation of both p44/p42 and p38 MAP kinases, implicated in mitogenic, inflammatory, and death-or survival-provoking pathways. [21][22][23][24] We examined these two MAP kinase family members, as recent studies elucidated specific roles for p44/p42 and p38 MAP kinase in podocyte stress. [25][26][27] In vivo, administration of inhibitors of these pathways to rodents receiving ADR attenuated proteinuria.…”

Section: Discussionmentioning

confidence: 99%

RAGE Mediates Podocyte Injury in Adriamycin-induced Glomerulosclerosis

Jiang¹,

Ananthakrishnan²,

Qu³

et al. 2008

Journal of the American Society of Nephrology

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In the kidney, the receptor for advanced glycation end products (RAGE) is principally expressed in the podocyte at low levels, but is upregulated in both human and mouse glomerular diseases. Because podocyte injury is central to proteinuric states, such as the nephrotic syndrome, the murine adriamycin nephrosis model was used to explore the role of RAGE in podocyte damage. In this model, administration of the anthracycline antibiotic adriamycin provokes severe podocyte stress and glomerulosclerosis. In contrast to wild-type animals, adriamycin-treated RAGE-null mice were significantly protected from effacement of the podocyte foot processes, albuminuria, and glomerulosclerosis. Administration of adriamycin induced rapid generation of RAGE ligands, and treatment with soluble RAGE protected against podocyte injury and glomerulosclerosis. In vitro, incubation of RAGE-expressing murine podocytes with adriamycin stimulated AGE formation, and treatment with RAGE ligands rapidly activated nicotinamide adenine dinucleotide phosphate (NADPH)-oxidase, via p44/p42 MAP kinase signaling, and upregulated pro-fibrotic growth factors. These data suggest that RAGE may contribute to the pathogenesis of podocyte injury in sclerosing glomerulopathies such as focal segmental glomerulosclerosis.

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“…1,2 Lack of apoptosis, with inappropriate cell proliferation in cancer is correlated with a high frequency of p53 mutations, in some tumours reaching 50%. Perhaps surprisingly, in view of the importance of p53 in regulating cell death and its strong phylogenetic conservation, only recently have homologous genes been identified.…”

mentioning

confidence: 99%

Additional complexity in p73: induction by mitogens in lymphoid cells and identification of two new splicing variants ε and ζ

et al. 1999

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Additional complexity in p73: induction by mitogens in lymphoid cells and identification of two new splicing variants e and z Dear Editor, p53 is a sequence specific transcription factor which transactivates several genes important in the apoptotic pathway, such as p21, mdm2, gadd45, bax and caspases. 1,2 Lack of apoptosis, with inappropriate cell proliferation in cancer is correlated with a high frequency of p53 mutations, in some tumours reaching 50%. Perhaps surprisingly, in view of the importance of p53 in regulating cell death and its strong phylogenetic conservation, only recently have homologous genes been identified.These (p63 and p73) show up to 63% aminoacid identity with p53 in the DNA binding, oligomerization and transcription activation domains, suggesting a similar mechanism of action to p53. 3±7 p63 is expressed as six different forms. 4 These use one of the two alternative transcription initiation sites, each transcript then being expressed as one of three alternatively spliced variants (a, b, g). Since the transcripts using the downstream ATG lack the first three exons coding for the transactivation domain, they act as natural dominant negative mutants of full length p63 and of p53. 4 The p73 gene comprises 14 exons and we have shown previously that in addition to the full length a form and the alternatively spliced transcript lacking exon 13 (b) other splice variants, lacking exon 11 (g) and exons 11, 12 and 13 (d) are also produced. 8 Stimulation of the T lymphoblastoid cell line, Jurkat, and human peripheral blood lymphocytes (PBL) with phytoemagglutinin (PHA) causes a 3 and 2.6-fold increase respectively in p73 expression by Northern blotting after 24 h (panel A). This is associated with induction of 34.7% and 21.2% of apoptotic cells respectively. No p53 was detected in Jurkat cells after PHA treatment (not shown).In order to discriminate the differential induction of the four p73 isoforms we performed an RT±PCR using isoformspecific primers on RNA extracted from cells treated under the same conditions. Panel B shows upregulation of a, b, g and d in PHA-treated PBL and Jurkat cells. Densitometric comparison of these with the housekeeping gene GAPDH showed that the increase in expression of each isoform were comparable (not shown).In addition, a new isoform was amplified from normal PBL. Cloning and sequencing of this p73e identified it as a splicing variant lacking exons 11 and 13 (panel C). To confirm the existence of p73e, we screened a panel of normal and tumour cell lines. As also shown in panel B, p73e was also present in the human hepatoma line HepG2, and a sixth isoform z was identified in the MCF7 human breast cancer cell line and in a human skin biopsy. p73 z is a further splice variant which lacks exons 11 and 12, and results in the loss of 96 aminoacids, the sequence continuing with the C-terminus of the a form (panel C). In p73e, loss of exon 11 deletes 50 aminoacids with a frame shift to the reading frame of the g isoform; splicing of exon 13 deletes an additional 31 aminoacids...

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Mechanism of UV-Induced Apoptosis in Human Leukemia Cells: Roles of Ca2+/Mg2+-Dependent Endonuclease, Caspase-3, and Stress-Activated Protein Kinases

Cited by 64 publications

References 53 publications

Triggering of Apoptosis is not Sufficient to Induce Human Immunodeficiency Virus Gene Expression

Triggering of Apoptosis is not Sufficient to Induce Human Immunodeficiency Virus Gene Expression

RAGE Mediates Podocyte Injury in Adriamycin-induced Glomerulosclerosis

Additional complexity in p73: induction by mitogens in lymphoid cells and identification of two new splicing variants ε and ζ

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