1301: An Exploratory Study of Cell Death Gene Changes After TBI in Novel RBM5 KO Mice

2020 ◽  
Vol 49 (1) ◽  
pp. 656-656
Author(s):  
Jeffrey Farooq ◽  
Keri Janesko-Feldman ◽  
Vincent Vagni ◽  
Kiersten Gorse ◽  
Patrick Kochanek ◽  
...  
Keyword(s):  
Cell Death ◽  
Exploratory Study ◽  
Cell Death Gene

Overexpression of bcl-xLProtects Astrocytes from Glucose Deprivation and Is Associated with Higher Glutathione, Ferritin, and Iron Levels 

1999 ◽  
Vol 91 (4) ◽  
pp. 1036-1036 ◽  
Author(s):  
Lijun Xu ◽  
Iphigenia L. Koumenis ◽  
Jonathan L. Tilly ◽  
Rona G. Giffard
Keyword(s):  
Hydrogen Peroxide ◽  
Cell Death ◽  
Glucose Deprivation ◽  
Normal Brain ◽  
Oxygen And Glucose Deprivation ◽  
Area Of Interest ◽  
Primary Astrocyte ◽  
Cell Death Gene ◽  
Antioxidant Effects ◽  
Normal Brain Development

Background The possibility of altering outcome from ischemia-like injury by overexpressing the anti-cell death gene bcl-xL was studied. Cells are known to die by different pathways including apoptosis, or programmed cell death, and necrosis. The bcl-xL gene is a member of a family of apoptosis regulating genes and often displays the death-inhibiting properties of the prototype of this family, bcl-2. It is of special interest to study bcl-xL for possible brain protection, because, unlike bcl-2, it is important for normal brain development. Methods Overexpression of bcl-xL was achieved in primary astrocyte cultures using a retroviral vector. Cultures of astrocytes overexpressing bcl-xL or a control gene were injured by hydrogen peroxide, glucose deprivation, or combined oxygen and glucose deprivation. Outcome was assessed morphologically and by release of lactate dehydrogenase. We assessed antioxidant effects by measuring glutathione using monochlorobimane, ferritin by immunoblotting, the level of iron spectrophotometrically, and superoxide using iodonitrotetrazolium violet and dihydroethidium. Results Protection by bcl-xL was found against glucose deprivation and hydrogen peroxide exposure but not combined oxygen and glucose deprivation. Higher levels of superoxide were found, without increased levels of lipid peroxidation. Overexpression of bcl-xL was associated with elevated glutathione levels, elevated ferritin levels, and increased amounts of iron. The increased glutathione contributed to the protection from glucose deprivation. Conclusions Overexpression of bcl-xL protects astrocytes from oxidative injury with the same spectrum of protection seen previously for bcl-2. The increased antioxidant defense observed should be beneficial against both apoptotic and necrotic cell death. The effects on levels of ferritin and iron are novel and identify a new area of interest for this gene family. Whether this relates to the effects of these genes on mitochondrial function remains to be elucidated.

Cell death gene expression profile: Role of RIPK2 in dengue virus-mediated apoptosis

2011 ◽  
Vol 156 (1-2) ◽  
pp. 25-34 ◽  
Author(s):  
Atthapan Morchang ◽  
Umpa Yasamut ◽  
Janjuree Netsawang ◽  
Sansanee Noisakran ◽  
Wiyada Wongwiwat ◽  
...  
Keyword(s):  
Gene Expression ◽  
Cell Death ◽  
Dengue Virus ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Cell Death Gene

scholarly journals A Cut/cohesin axis alters the chromatin landscape to facilitate neuroblast death

2018 ◽  
Author(s):  
Richa Arya ◽  
Seda Gyonjyan ◽  
Katherine Harding ◽  
Tatevik Sarkissian ◽  
Ying Li ◽  
...  
Keyword(s):  
Gene Expression ◽  
Stem Cells ◽  
Cell Death ◽  
Nervous System ◽  
Neural Stem Cells ◽  
Open Chromatin ◽  
Chromatin Conformation ◽  
Precise Control ◽  
Cell Death Gene ◽  
Cell Death Genes

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.

scholarly journals Programmed cell death takes flight: genetic and genomic approaches to gene discovery in Drosophila

2002 ◽  
Vol 9 (2) ◽  
pp. 59-69 ◽  
Author(s):  
S. Gorski ◽  
M. Marra
Keyword(s):  
Cell Death ◽  
Drosophila Melanogaster ◽  
Programmed Cell Death ◽  
Gene Discovery ◽  
Fruit Fly ◽  
Model System ◽  
Physiological Process ◽  
Wide Spread ◽  
Cell Death Gene ◽  
Genetics And Genomics

Programmed cell death (PCD) is an essential and wide-spread physiological process that results in the elimination of cells. Genes required to carry out this process have been identified, and many of these remain the subjects of intense investigation. Here, we describe PCD, its functions, and some of the consequences when it goes awry. We review PCD in the model system, the fruit fly, Drosophila melanogaster, with a particular emphasis on cell death gene discovery resulting from both genetics and genomics-based approaches.

scholarly journals Functional role of interleukin 1 beta (IL-1 beta) in IL-1 beta-converting enzyme-mediated apoptosis.

1996 ◽  
Vol 184 (2) ◽  
pp. 717-724 ◽  
Author(s):  
R M Friedlander ◽  
V Gagliardini ◽  
R J Rotello ◽  
J Yuan
Keyword(s):  
Cell Death ◽  
Neutralizing Antibodies ◽  
Interleukin 1 ◽  
Interleukin 1 Beta ◽  
Converting Enzyme ◽  
Necrosis Factor Alpha ◽  
Trophic Factor Deprivation ◽  
Cell Death Gene ◽  
Factor Alpha ◽  
Induced Apoptosis

Prointerleukin-1 beta (pro-IL-1 beta) is the only known physiologic substrate of the interleukin-1 beta (IL-1 beta)-converting enzyme (ICE), the founding member of the ICE/ced-3 cell death gene family. Since secreted mature IL-1 beta has been detected after apoptosis, we investigated whether this cytokine, when produced endogenously, plays a role in cell death. We found that hypoxia-induced apoptosis can be inhibited by either the IL-1 receptor antagonist (IL-1Ra) or by neutralizing antibodies to IL-1 or to its type 1 receptor. IL-1Ra also inhibits apoptosis induced by trophic factor deprivation in primary neurons, as well as by tumor necrosis factor alpha in fibroblasts. In addition, during the G1/S phase arrest, mature IL-1 beta induces apoptosis through a pathway independent of CrmA-sensitive gene activity. We also demonstrate that Ice, when expressed in COS cells, requires the coexpression of pro-IL-1 beta for the induction of apoptosis, which is inhibited by IL-1Ra. Interestingly, we found that mature IL-1 beta has antiapoptotic activity when added exogenously before the onset of hypoxia, which we found is caused in part by its ability to downregulate the IL-1 receptor. Our findings demonstrate that pro-IL-1 beta is a substrate of ICE relevant to cell death, and depending on the temporal cellular commitment to apoptosis, mature IL-1 beta may function as a positive or negative mediator of cell death.

Sign in / Sign up

Export Citation Format

Share Document