scholarly journals Sensitive-stage embryo irradiation affects embryonic neuroblasts and adult motor function

Author(s):  
Ram Wagle ◽  
Young-Han Song

Abstract Background Cranial radiation therapy for treating childhood malignancies in the central nervous system or accidental radiation exposure may result in neurological side effects in surviving adults. As tissue homeostasis is maintained by stem cells, understanding the effect of radiation on neural stem cells will provide clues for managing the neurological effects. Drosophila embryos were used as a model system whose sensitivity to irradiation-induced cell death changes from the sensitive to resistant stage during development. Objective Drosophila embryos at the radiation-sensitive stage were irradiated at various doses and the radiation sensitivity was tested regarding the appearance of apoptotic cells in the embryos and the embryonic lethality. Cell fates of the neural stem cells called neuroblasts (NBs) and adult motor function after irradiation were also investigated. Result Irradiation of Drosophila embryos at the radiation-sensitive stage resulted in a dose-dependent increase in the number of embryos containing apoptotic cells 75 min after treatment starting at 3 Gy. Embryonic lethality assayed by hatch rate was induced by 1 Gy irradiation, which did not induce cell death. Notably, no apoptosis was detected in NBs up to 2 h after irradiation at doses as high as 40 Gy. At 3 h after irradiation, as low as 3 Gy, the number of NBs marked by Dpn and Klu was decreased by an unidentified mechanism regardless of the cell death status of the embryo. Furthermore, embryonic irradiation at 3 Gy, but not 1 Gy, resulted in locomotor defects in surviving adults. Conclusion Embryonic NBs survived irradiation at doses as high as 40 Gy, while cells in other parts of the embryos underwent apoptosis at doses higher than 3 Gy within 2 h after treatment. Three hours after exposure to a minimum dose of 3 Gy, the number of NBs marked by Dpn and Klu decreased, and the surviving adults exhibited defects in locomotor ability.

2003 ◽  
Vol 144 ◽  
pp. s11 ◽  
Author(s):  
S. Ceccatelli ◽  
C. Tamm ◽  
E. Sleeper ◽  
S. Orrenius ◽  
E.Y. Snyder

2014 ◽  
Vol 1843 (6) ◽  
pp. 1162-1171 ◽  
Author(s):  
Kin Pong U ◽  
Venkataraman Subramanian ◽  
Antony P. Nicholas ◽  
Paul R. Thompson ◽  
Patrizia Ferretti

2017 ◽  
Vol 45 (1) ◽  
pp. 108-118 ◽  
Author(s):  
Qingsong Ye ◽  
Yanqing Wu ◽  
Jiamin Wu ◽  
Shuang Zou ◽  
Ali Ahmed Al-Zaazaai ◽  
...  

Background/Aims: Neonatal hypoxia-ischemia (HI) causes severe brain damage and significantly increases neonatal morbidity and mortality. Increasing evidences have verified that stem cell-based therapy has the potential to rescue the ischemic tissue and restore function via secreting growth factors after HI. Here, we had investigated whether intranasal neural stem cells (NSCs) treatment improves the recovery of neonatal HI, and NSCs overexpressing basic fibroblast growth factor (bFGF) has a better therapeutic effect for recovery than NSCs treatment only. Methods: We performed permanent occlusion of the right common carotid artery in 9-day old ICR mice as animal model of neonatal hypoxia-ischemia. At 3 days post-HI, NSC, NSC-GFP, NSC-bFGF and vehicle were delivered intranasally. To determine the effect of intranasal NSC, NSC-GFP and NSC-bFGF treatment on recovery after HI, we analyzed brain damage, sensor-motor function and cell differentiation. Results: It was observed that intranasal NSC, NSC-GFP and NSC-bFGF treatment decreased gray and white matter loss area in comparison with vehicle-treated mouse. NSC, NSC-GFP and NSC-bFGF treatment also significantly improved sensor motor function in cylinder rearing test and adhesive removal test, however, NSC-bFGF-treatment was more effective than NSC-treatment in the improvement of somatosensory function. Furthermore, compared with NSC and NSC-GFP, NSC-bFGF treatment group appeared to differentiate into more neurons. Conclusion: Taken together, intranasal administration of NSCs is a promising therapy for treatment of neonatal HI, but NSCs overexpressing bFGF promotes the survival and differentiation of NSCs, and consequently achieves a better therapeutic effect in improving recovery after neonatal HI.


Author(s):  
Hyunhee Park ◽  
Kyung Min Chung ◽  
Hyun-Kyu An ◽  
Ji-Eun Gim ◽  
Jihyun Hong ◽  
...  

2004 ◽  
Vol 83 (2) ◽  
pp. 313-328 ◽  
Author(s):  
Jiang Li ◽  
Delinda Johnson ◽  
Marcus Calkins ◽  
Lynda Wright ◽  
Clive Svendsen ◽  
...  

2012 ◽  
Vol 22 (2) ◽  
pp. 127-137 ◽  
Author(s):  
Henricus A. M. Mutsaers ◽  
Roshan Tofighi

2018 ◽  
Author(s):  
Richa Arya ◽  
Seda Gyonjyan ◽  
Katherine Harding ◽  
Tatevik Sarkissian ◽  
Ying Li ◽  
...  

AbstractPrecise control of cell death in the nervous system is essential for development. Spatial and temporal factors activate the death of Drosophila neural stem cells (neuroblasts) by controlling the transcription of multiple cell death genes through a shared enhancer, enh1. The activity of enh1 is controlled by abdominalA and Notch, but additional inputs are needed for proper specificity. Here we show that the Cut DNA binding protein is required for neuroblast death, acting downstream of enh1. In the nervous system, Cut promotes an open chromatin conformation in the cell death gene locus, allowing cell death gene expression in response to abdominalA. We demonstrate a temporal increase in global H3K27me3 levels in neuroblasts, which is enhanced by cut knockdown. Furthermore, cut regulates the expression of the cohesin subunit Stromalin in the nervous system. The cohesin components Stromalin and NippedB are required for neuroblast death, and knockdown of Stromalin increases repressive histone modifications in neuroblasts. Thus Cut and cohesin regulate apoptosis in the developing nervous system by altering the chromatin landscape.Summary statementCut regulates the programmed death of neural stem cells by altering cohesin levels and promoting a more open chromatin conformation to allow cell death gene expression.


2018 ◽  
Vol 59 (5) ◽  
pp. 203-212
Author(s):  
Valentina Hribljan ◽  
Iva Salamon ◽  
Arijana Đemaili ◽  
Ivan Alić ◽  
Dinko Mitrečić

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