Selective blockade of CaMKII-α inhibits NMDA-induced caspase-3-dependent cell death but does not arrest PARP-1 activation or loss of plasma membrane selectivity in rat retinal neurons

2009 ◽  
Vol 1256 ◽  
pp. 190-204 ◽  
Author(s):  
Dennis J. Goebel
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Caspase 3 ◽  
Retinal Neurons ◽  
Membrane Selectivity ◽  
Selective Blockade ◽  
Dependent Cell ◽  
Parp 1

scholarly journals CMPG1-dependent cell death follows perception of diverse pathogen elicitors at the host plasma membrane and is suppressed by Phytophthora infestans RXLR effector AVR3a

2011 ◽  
Vol 190 (3) ◽  
pp. 653-666 ◽  
Author(s):  
Eleanor M. Gilroy ◽  
Rosalind M. Taylor ◽  
Ingo Hein ◽  
Petra Boevink ◽  
Ari Sadanandom ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Phytophthora Infestans ◽  
Rxlr Effector ◽  
Host Plasma Membrane ◽  
Dependent Cell

scholarly journals Blockage of NOX2/MAPK/NF-κB Pathway Protects Photoreceptors against Glucose Deprivation-Induced Cell Death

2017 ◽  
Vol 2017 ◽  
pp. 1-14 ◽  
Author(s):  
Bin Fan ◽  
Bei-Fen Wang ◽  
Lin Che ◽  
Ying-Jian Sun ◽  
Shu-Yan Liu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Western Blot ◽  
Glucose Deprivation ◽  
Photoreceptor Cells ◽  
Retinal Neurons ◽  
Dependent Cell ◽  
Ischemic Diseases ◽  
Cell Death Cascade ◽  
Energy Failure

Acute energy failure is one of the critical factors contributing to the pathogenic mechanisms of retinal ischemia. Our previous study demonstrated that glucose deprivation can lead to a caspase-dependent cell death of photoreceptors. The aim of this study was to decipher the upstream signal pathway in glucose deprivation- (GD-) induced cell death. We mimicked acute energy failure by using glucose deprivation in photoreceptor cells (661W cells). GD-induced oxidative stress was evaluated by measuring ROS with the DCFH-DA assay and HO-1 expression by Western blot analysis. The activation of NOX2/MAPK/NF-κB signal was assessed by Western blot and immunohistochemical assays. The roles of these signals in GD-induced cell death were measured by using their specific inhibitors. Inhibition of Rac-1 and NOX2 suppressed GD-induced oxidative stress and protected photoreceptors against GD-induced cell death. NOX2 was an upstream signal in the caspase-dependent cell death cascade, yet the downstream MAPK pathways were activated and blocking MAPK signals rescued 661W cells from GD-induced death. In addition, GD caused the activation of NF-κB signal and inhibiting NF-κB significantly protected 661W cells. These observations may provide insights for treating retinal ischemic diseases and protecting retinal neurons from ischemia-induced cell death.

Ethanol Enhances Activation-Induced Caspase-3 Dependent Cell Death in T Lymphocytes

2002 ◽  
Vol 26 (3) ◽  
pp. 363-370 ◽  
Author(s):  
Sujata Kelkar ◽  
Qing Dong ◽  
Yinghua Xiao ◽  
Swati Joshi-Barve ◽  
Craig J. McClain ◽  
...  
Keyword(s):  
Cell Death ◽  
T Lymphocytes ◽  
Caspase 3 ◽  
Dependent Cell

Ethanol Enhances Activation-Induced Caspase-3 Dependent Cell Death in T Lymphocytes

2002 ◽  
Vol 26 (3) ◽  
pp. 363-370
Author(s):  
Sujata Kelkar ◽  
Qing Dong ◽  
Yinghua Xiao ◽  
Swati Joshi-Barve ◽  
Craig J. McClain ◽  
...  
Keyword(s):  
Cell Death ◽  
T Lymphocytes ◽  
Caspase 3 ◽  
Dependent Cell

scholarly journals AEBP1 down regulation induced cell death pathway depends on PTEN status of glioma cells

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Swati Sinha ◽  
Arun Renganathan ◽  
Prathima B. Nagendra ◽  
Vasudeva Bhat ◽  
Brian Steve Mathew ◽  
...  
Keyword(s):  
Dna Damage ◽  
Cell Death ◽  
Cellular Proliferation ◽  
Ectopic Expression ◽  
Glioma Cells ◽  
Down Regulation ◽  
Over Expression ◽  
Cell Death Pathway ◽  
Dependent Cell ◽  
Parp 1

Abstract Glioblastoma (GBM) is the most common aggressive form of brain cancer with overall dismal prognosis (10–12 months) despite all current multimodal treatments. Previously we identified adipocyte enhancer binding protein 1 (AEBP1) as a differentially regulated gene in GBM. On probing the role of AEBP1 over expression in glioblastoma, we found that both cellular proliferation and survival were affected upon AEBP1 silencing in glioma cells, resulting in cell death. In the present study we report that the classical caspase pathway components are not activated in cell death induced by AEBP1 down regulation in PTEN-deficient (U87MG and U138MG) cells. PARP-1 was not cleaved but over-activated under AEBP1 down regulation which leads to the synthesis of PAR in the nucleus triggering the release of AIF from the mitochondria. Subsequently, AIF translocates to the nucleus along with MIF causing chromatinolysis. AEBP1 positively regulates PI3KinaseCβ by the binding to AE-1 binding element in the PI3KinaseCβ promoter. Loss of PI3KinaseCβ expression under AEBP1 depleted condition leads to excessive DNA damage and activation of PARP-1. Furthermore, over expression of PIK3CB (in trans) in U138MG cells prevents DNA damage in these AEBP1 depleted cells. On the contrary, AEBP1 down regulation induces caspase-dependent cell death in PTEN-proficient (LN18 and LN229) cells. Ectopic expression of wild-type PTEN in PTEN-deficient U138MG cells results in the activation of canonical caspase and Akt dependent cell death. Collectively, our findings define AEBP1 as a potential oncogenic driver in glioma, with potential implications for therapeutic intervention.

scholarly journals The neuroprotective effect of nicotine in Parkinson’s disease models is associated with inhibiting PARP-1 and caspase-3 cleavage

PeerJ ◽  
2017 ◽  
Vol 5 ◽  
pp. e3933 ◽  
Author(s):  
Justin Y.D. Lu ◽  
Ping Su ◽  
James E.M. Barber ◽  
Joanne E. Nash ◽  
Anh D. Le ◽  
...  
Keyword(s):  
Parkinson’S Disease ◽  
Parkinson's Disease ◽  
Cell Death ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Future Research ◽  
Neuroprotective Effects ◽  
Α7 Nachr ◽  
Parp 1

Clinical evidence points to neuroprotective effects of smoking in Parkinson’s disease (PD), but the molecular mechanisms remain unclear. We investigated the pharmacological pathways involved in these neuroprotective effects, which could provide novel ideas for developing targeted neuroprotective treatments for PD. We used the ETC complex I inhibitor methylpyridinium ion (MPP+) to induce cell death in SH-SY5Y cells as a cellular model for PD and found that nicotine inhibits cell death. Using choline as a nicotinic acetylcholine receptor (nAChR) agonist, we found that nAChR stimulation was sufficient to protect SH-SY5Y cells against cell death from MPP+. Blocking α7 nAChR with methyllycaconitine (MLA) prevented the protective effects of nicotine, demonstrating that these receptors are necessary for the neuroprotective effects of nicotine. The neuroprotective effect of nicotine involves other pathways relevant to PD. Cleaved Poly (ADP-ribose) polymerase-1 (PARP-1) and cleaved caspase-3 were decreased by nicotine in 6-hydroxydopamine (6-OHDA) lesioned mice and in MPP+-treated SH-SY5Y cells. In conclusion, our data indicate that nicotine likely exerts neuroprotective effects in PD through the α7 nAChR and downstream pathways including PARP-1 and caspase-3. This knowledge could be pursued in future research to develop neuroprotective treatments for PD.

scholarly journals Procaspase-activating compound 1 induces a caspase-3-dependent cell death in cerebellar granule neurons

2010 ◽  
Vol 247 (3) ◽  
pp. 238-242 ◽  
Author(s):  
Gulzeb Aziz ◽  
Øyvind W. Akselsen ◽  
Trond V. Hansen ◽  
Ragnhild E. Paulsen
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Cerebellar Granule Neurons ◽  
Granule Neurons ◽  
Cerebellar Granule ◽  
Dependent Cell
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