scholarly journals CXCR4 increases in-vivo glioma perivascular invasion, and reduces radiation induced apoptosis: A genetic knockdown study

Oncotarget ◽  
2016 ◽  
Vol 7 (50) ◽  
pp. 83701-83719 ◽  
Author(s):  
Viveka Nand Yadav ◽  
Daniel Zamler ◽  
Gregory J. Baker ◽  
Padma Kadiyala ◽  
Anat Erdreich-Epstein ◽  
...  
Keyword(s):  
Radiation Induced ◽  
Perivascular Invasion ◽  
Induced Apoptosis

scholarly journals DR5 Knockout Mice Are Compromised in Radiation-Induced Apoptosis

2005 ◽  
Vol 25 (5) ◽  
pp. 2000-2013 ◽  
Author(s):  
Niklas Finnberg ◽  
Joshua J. Gruber ◽  
Peiwen Fei ◽  
Dorothea Rudolph ◽  
Anka Bric ◽  
...  
Keyword(s):  
Cell Death ◽  
Null Mouse ◽  
Organ Specific ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
The Brain ◽  
Necrosis Factor

ABSTRACT DR5 (also called TRAIL receptor 2 and KILLER) is an apoptosis-inducing membrane receptor for tumor necrosis factor-related apoptosis-inducing ligand (also called TRAIL and Apo2 ligand). DR5 is a transcriptional target of p53, and its overexpression induces cell death in vitro. However, the in vivo biology of DR5 has remained largely unexplored. To better understand the role of DR5 in development and in adult tissues, we have created a knockout mouse lacking DR5. This mouse is viable and develops normally with the exception of having an enlarged thymus. We show that DR5 is not expressed in developing embryos but is present in the decidua and chorion early in development. DR5-null mouse embryo fibroblasts expressing E1A are resistant to treatment with TRAIL, suggesting that DR5 may be the primary proapoptotic receptor for TRAIL in the mouse. When exposed to ionizing radiation, DR5-null tissues exhibit reduced amounts of apoptosis compared to wild-type thymus, spleen, Peyer's patches, and the white matter of the brain. In the ileum, colon, and stomach, DR5 deficiency was associated with a subtle phenotype of radiation-induced cell death. These results indicate that DR5 has a limited role during embryogenesis and early stages of development but plays an organ-specific role in the response to DNA-damaging stimuli.

scholarly journals Relationship of Doxorubicin- and Radiation-Induced Apoptosis with Ki-67 Labeling Index in Human Tumors in vivo.

1999 ◽  
Vol 49 (6) ◽  
pp. 431-435
Author(s):  
Kayoko Hayakawa ◽  
Masatoshi Hasegawa ◽  
Miho Kawashima ◽  
Hisako Toda ◽  
Kazushige Hayakawa ◽  
...  
Keyword(s):  
Human Tumors ◽  
Labeling Index ◽  
Ki 67 ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
Relationship Of

In vivo imaging of radiation-induced apoptosis in follicular lymphoma patients

2004 ◽  
Vol 59 (3) ◽  
pp. 782-787 ◽  
Author(s):  
Rick L.M Haas ◽  
Daphne de Jong ◽  
Renato A Valdés Olmos ◽  
Cees A Hoefnagel ◽  
Iris van Den Heuvel ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
In Vivo Imaging ◽  
Radiation Induced ◽  
Induced Apoptosis

2001 p53-Dependent radiation-induced apoptosis in vivo: Relationship to Bcl-2 and Bax expression

1997 ◽  
Vol 39 (2) ◽  
pp. 241
Author(s):  
Masatoshi Hasegawa ◽  
Yoshiyuki Suzuki ◽  
Masaya Furuta ◽  
Michitaka Yamakawa ◽  
Katsuya Maebayashi ◽  
...  
Keyword(s):  
Radiation Induced ◽  
Induced Apoptosis

710 In vivo assessment of radiation induced apoptosis in follicular lymphoma patients by 99mTc-Annexin V scintigraphy

2003 ◽  
Vol 1 (5) ◽  
pp. S214
Author(s):  
R.L.M. Haas ◽  
R.A. Valdés-Olmos ◽  
D. de Jong ◽  
S.F. Zerp ◽  
I. van den Heuvel ◽  
...  
Keyword(s):  
Follicular Lymphoma ◽  
Annexin V ◽  
Radiation Induced ◽  
Induced Apoptosis ◽  
In Vivo Assessment

scholarly journals Substituted Piperazines as Novel Potential Radioprotective Agents

Molecules ◽  
2020 ◽  
Vol 25 (3) ◽  
pp. 532
Author(s):  
Alzbeta Filipova ◽  
Jan Marek ◽  
Radim Havelek ◽  
Jaroslav Pejchal ◽  
Marcela Jelicova ◽  
...  
Keyword(s):  
Whole Body ◽  
Piperazine Derivatives ◽  
Radiation Induced ◽  
Low Toxicity ◽  
Increasing Risk ◽  
Low Cytotoxicity ◽  
Induced Apoptosis ◽  
Previous Series

The increasing risk of radiation exposure underlines the need for novel radioprotective agents. Hence, a series of novel 1-(2-hydroxyethyl)piperazine derivatives were designed and synthesized. Some of the compounds protected human cells against radiation-induced apoptosis and exhibited low cytotoxicity. Compared to the previous series of piperazine derivatives, compound 8 exhibited a radioprotective effect on cell survival in vitro and low toxicity in vivo. It also enhanced the survival of mice 30 days after whole-body irradiation (although this increase was not statistically significant). Taken together, our in vitro and in vivo data indicate that some of our compounds are valuable for further research as potential radioprotectors.

scholarly journals Activation of guanylate cyclase C signaling pathway protects intestinal epithelial cells from acute radiation-induced apoptosis

2009 ◽  
Vol 296 (4) ◽  
pp. G740-G749 ◽  
Author(s):  
M. P. Garin-Laflam ◽  
K. A. Steinbrecher ◽  
J. A. Rudolph ◽  
J. Mao ◽  
M. B. Cohen
Keyword(s):  
Guanylate Cyclase ◽  
Peptide Hormone ◽  
In Vivo Model ◽  
Proximal Jejunum ◽  
Intestinal Epithelial ◽  
Γ Irradiation ◽  
Guanylate Cyclase C ◽  
Radiation Induced ◽  
Induced Apoptosis

Uroguanylin (UGN) is a peptide hormone that binds to and activates the intestinal epithelial cell (IEC) transmembrane receptor guanylate cyclase C (GC-C), which in turn increases intracellular cGMP. Gene targeting of murine UGN or GC-C results in significantly lower levels of cGMP in IECs. On the basis of effects of cGMP in nonintestinal systems, we hypothesized that loss of GC-C activation would increase intestinal epithelial apoptosis following radiation-induced injury. We first compared apoptosis from the proximal jejunum of C57BL/6 wild-type (WT) and GC-C knockout (KO) mice 3 h after they received 5 Gy of γ-irradiation. We then investigated whether supplementation via intraperitoneal injection of 1 mM 8BrcGMP would mitigate radiation-induced apoptosis in these experimental animals. Identical experiments were performed in BALB/c UGN WT and KO mice. Apoptosis was assessed by quantitating morphological indications of cell death, terminal dUTP nick-end labeling, and cleaved caspase 3 immunohistochemistry. Both UGN KO and GC-C KO mice were more susceptible than their WT littermates in this in vivo model of apoptotic injury. Furthermore, cGMP supplementation in both GC-C and UGN KO animals ameliorated radiation-induced apoptosis. Neither WT strain demonstrated significant alteration in apoptotic susceptibility as a result of cGMP supplementation before radiation injury. These in vivo findings demonstrate increased radiosensitivity of IECs in UGN and GC-C KO mice and a role for cGMP as a primary downstream mediator of GC-C activation in the protection of these IECs from radiation-induced apoptosis.

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