Quantitative Proteome Analysis Reveals RNA Processing Factors As Modulators of Ionizing Radiation-Induced Apoptosis in the C. elegans Germline.

2012 ◽  
Vol 11 (8) ◽  
pp. 4277-4288 ◽  
Author(s):  
Gisele G. Tomazella ◽  
Henok Kassahun ◽  
Hilde Nilsen ◽  
Bernd Thiede
Keyword(s):  
Ionizing Radiation ◽  
Rna Processing ◽  
Proteome Analysis ◽  
C Elegans ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Processing Factors

Granulocyte-Macrophage Colony-Stimulating Factor Rescues TF-1 Leukemia Cells From Ionizing Radiation-Induced Apoptosis Through a Pathway Mediated by Protein Kinase Cα

Blood ◽  
1998 ◽  
Vol 92 (2) ◽  
pp. 416-424 ◽  
Author(s):  
Mary L. Kelly ◽  
Yan Tang ◽  
Nitsa Rosensweig ◽  
Sanda Clejan ◽  
Barbara S. Beckman
Keyword(s):  
Protein Kinase ◽  
Ionizing Radiation ◽  
Colony Stimulating Factor ◽  
Gm Csf ◽  
Pkc Isoforms ◽  
Radiation Induced ◽  
Macrophage Colony Stimulating Factor ◽  
Macrophage Colony ◽  
Induced Apoptosis ◽  
Stimulating Factor

Abstract Protein kinase C (PKC) activity has a recognized role in mediating apoptosis. However, the role of individual PKC isoforms in apoptosis is poorly defined. Therefore, we investigated the translocation of individual PKC isoforms during radiation-induced apoptosis with and without rescue from apoptosis by granulocyte-macrophage colony-stimulating factor (GM-CSF) in the human erythroleukemia cell line TF-1. PKCα was translocated from the particulate to cytosolic fraction of TF-1 cells within 5 minutes of treatment with apoptosis-inducing levels of ionizing radiation. However, this postirradiation translocation did not occur when cells were rescued from apoptosis by GM-CSF. Furthermore, treatment of cells with Gö6976, an inhibitor of classical PKC isoforms, abrogated the rescue effect of GM-CSF. The calcium-independent novel PKC isoform, PKCδ appeared to be degraded in both the particulate and cytosolic fractions of TF-1 cells after treatment with apoptosis-inducing levels of ionizing radiation in either the presence or absence of GM-CSF rescue. Levels of ceramide, a lipid mediator of apoptosis, were measured at 2, 4, 8, 10, and 60 minutes after treatment with ionizing radiation and were substantially reduced in TF-1 cells rescued from apoptosis by GM-CSF compared with apoptotic TF-1 cells. The largest decrease in ceramide production seen was at 4 minutes postirradiation, with a 46% reduction in ceramide levels in TF-1 cells rescued from apoptosis by GM-CSF compared with those in apoptotic TF-1 cells. Because ceramide has been shown to affect PKCα subcellular distribution, these data implicate a role for ceramide in mediating the rapid postirradiation translocation and inhibition of PKCα in TF-1 cells not rescued from apoptosis by GM-CSF. Expression of the antiapoptotic protein Bcl-2 doubled in TF-1 cells rescued from apoptosis by GM-CSF, but did not increase in unrescued cells. Our findings suggest that activated PKCα and increased expression of Bcl-2 after γ irradiation determine survival in TF-1 cells rescued from apoptosis with GM-CSF and that PKCδ plays a role in mediating signals involved in sensing cellular damage and/or regulation of cell damage repair.

scholarly journals Catalase Inhibits Ionizing Radiation-Induced Apoptosis in Hematopoietic Stem and Progenitor Cells

2015 ◽  
Vol 24 (11) ◽  
pp. 1342-1351 ◽  
Author(s):  
Xia Xiao ◽  
Hongmei Luo ◽  
Kenneth N. Vanek ◽  
Amanda C. LaRue ◽  
Bradley A. Schulte ◽  
...  
Keyword(s):  
Ionizing Radiation ◽  
Progenitor Cells ◽  
Hematopoietic Stem ◽  
Stem And Progenitor Cells ◽  
Radiation Induced ◽  
Induced Apoptosis

PS-341–mediated selective targeting of multiple myeloma cells by synergistic increase in ionizing radiation-induced apoptosis

2005 ◽  
Vol 33 (7) ◽  
pp. 784-795 ◽  
Author(s):  
Apollina Goel ◽  
Angela Dispenzieri ◽  
Philip R. Greipp ◽  
Thomas E. Witzig ◽  
Ruben A. Mesa ◽  
...  
Keyword(s):  
Multiple Myeloma ◽  
Ionizing Radiation ◽  
Myeloma Cells ◽  
Selective Targeting ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Synergistic Increase

Modification of radiation-induced apoptosis in radiation- or hyperthermia-adapted human lymphocytes

1994 ◽  
Vol 72 (11-12) ◽  
pp. 475-482 ◽  
Author(s):  
S. P. Cregan ◽  
D. R. Boreham ◽  
P. R. Walker ◽  
D. L. Brown ◽  
R. E. J. Mitchel
Keyword(s):  
Dna Damage ◽  
Ionizing Radiation ◽  
Adaptive Response ◽  
Human Peripheral Blood ◽  
Human Lymphocytes ◽  
Fluorescence Analysis ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Protective Mechanism ◽  
Radiation Induced ◽  
Induced Apoptosis

We have investigated the influence of the cellular adaptive response to ionizing radiation on radiation-induced apoptosis in human cells. The adaptive response is believed to be a protective mechanism that confers resistance to the detrimental effects of ionizing radiation and that can be induced by different agents, including hyperthermia and radiation. We have used fluorescence analysis of DNA unwinding (FADU) to assay the induction of apoptosis in human peripheral blood lymphocytes by ionizing radiation. Using the FADU assay, we have observed the initial radiation-induced DNA damage, its subsequent disappearance due to enzymatic repair, and its time- and dose-dependent reappearance. We believe this reappearance of DNA damage to be indicative of the DNA fragmentation event associated with apoptosis. This interpretation has been supported at the individual cell level using an in situ terminal deoxynucleotidyl transferase (TDT) assay (Apoptag, Oncor Inc.), which detects the 3′-hydroxyl ends of fragmented DNA, and by fluorescence analysis of nuclear morphology in Hoechst 33258 stained cells. Pretreatment of cells with low-dose γ-radiation (0.1 Gy) or mild hyperthermia (40 °C for 30 min) altered the extent of radiation-induced (3 Gy) apoptosis. Both pretreatments sensitized lymphocytes to become apoptotic after the 3-Gy radiation exposure. This sensitization may represent an adaptive response mechanism that reduces the risk that genetically damaged cells will proliferate. The ability to modify the probability of radiation-induced apoptosis may lower the cancer risk from a radiation exposure.Key words: apoptosis, adaptive response, ionizing radiation, hyperthermia.

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