A new technique for real-time analysis of caspase-3 dependent neuronal cell death

2007 ◽  
Vol 161 (2) ◽  
pp. 234-243 ◽  
Author(s):  
Antje Golbs ◽  
Nicolas Heck ◽  
Heiko J. Luhmann
Keyword(s):  
Cell Death ◽  
Real Time ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
New Technique ◽  
Time Analysis ◽  
Real Time Analysis ◽  
A New Technique

scholarly journals Neurotoxic Effect of Ethanolic Extract of Propolis in the Presence of Copper Ions is Mediated through Enhanced Production of ROS and Stimulation of Caspase-3/7 Activity

Toxins ◽  
2019 ◽  
Vol 11 (5) ◽  
pp. 273 ◽  
Author(s):  
Vedrana Radovanović ◽  
Josipa Vlainić ◽  
Nikolina Hanžić ◽  
Petra Ukić ◽  
Nada Oršolić ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Damage ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Ethanolic Extract ◽  
Mitogen Activated Protein Kinase ◽  
Enhanced Production ◽  
Toxicological Studies ◽  
Ethanolic Extract Of Propolis

Elevated amounts of copper are considered to be contributing factor in the progression of neurodegenerative diseases as they promote oxidative stress conditions. The aim of our study was to examine the effects of ethanolic extract of propolis (EEP) against copper-induced neuronal damage. In cultured P19 neuronal cells, EEP exacerbated copper-provoked neuronal cell death by increasing the generation of reactive oxygen species (ROS) and through the activation of caspase-3/7 activity. EEP augmented copper-induced up-regulation of p53 and Bax mRNA expressions. Neurotoxic effects of EEP were accompanied by a strong induction of glyceraldehyde 3-phosphate dehydrogenase (GAPDH) expression and decrease in the expression of c-fos mRNA. SB203580, an inhibitor of p38 mitogen-activated protein kinase (MAPK) prevented detrimental effects of EEP, whereas SP600125, an inhibitor of c-Jun N-terminal kinase (JNK), exacerbated EEP-induced neuronal cell death. Quercetin, a polyphenolic nutraceutical, which is usually present in propolis, was also able to exacerbate copper-induced neuronal death. Our data indicates a pro-oxidative and apoptotic mode of EEP action in the presence of excess copper, wherein ROS/p53/p38 interactions play an important role in death cascades. Our study also pointed out that detailed pharmacological and toxicological studies must be carried out for propolis and other dietary supplements in order to fully recognize the potential adverse effects in specific conditions.

Role of caspase-3 in neuronal cell death

1998 ◽  
Vol 5 ◽  
pp. 207
Author(s):  
A. Gorman ◽  
E. Bonfoco ◽  
B. Zhivotovsky ◽  
S. Orrenius ◽  
S. Ceccatelli
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

scholarly journals Caspase-3-Like Protease Activity-Independent Apoptosis at the Onset of Neuronal Cell Death in the Gerbil Hippocampus after Global Ischemia

2007 ◽  
Vol 30 (10) ◽  
pp. 1950-1953 ◽  
Author(s):  
Hiroki Shimizu ◽  
Makoto Ohgoh ◽  
Masuhiro Ikeda ◽  
Yukio Nishizawa ◽  
Hiroo Ogura
Keyword(s):  
Cell Death ◽  
Protease Activity ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Global Ischemia

scholarly journals The Efficacy of Cinnamomum burmanii Extract on the Protection of Neuronal Cell Death in Haloperidol Induced Male Wistar Rats

2018 ◽  
Vol 2 (4) ◽  
pp. 1-11
Author(s):  
Nita Parisa ◽  
MT Kamaluddin ◽  
Theodorus Theodorus
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Positive Control ◽  
Control Group ◽  
Cinnamon Extract ◽  
White Rats ◽  
Before And After ◽  
Mean Differences

Background Haloperidol is categorized as the first class antipsychotic drug. Long-term use of haloperidol may convey to increased Reactive Oxygen Species (ROS) that will yield oxidative damage which further leads to cell death. Several studies had identified the effects of cinnamon extract on cell death. This study aimed to determine the efficacy of cinnamon extract (Cinnamomum burmanii) on the protection of neuronal cell death in haloperidol-induced male Wistar white rats. Methods This study was experimental with pre and post-test design. Thirty male Wistar rats were divided into 5 groups, induced with haloperidol and followed by treatment. Caspase-3 and dopamine were assayed by ELISA sandwich method using ELISA kit. Mean difference of caspase expression and dopamine levels before and after induction were shown (p<0.05). Results There were mean differences of caspase-3 expression level in the positive control group, cinnamon extract of 100 and 200mg/kgBW before and after treatment (p<0.05). Whereas for dopamine levels, there were mean differences in positive control group, cinnamon extract of 50, 100 and 200mg/kgBW before and after treatment (p<0.05). With Post Hoc test, it was found that there were no mean differences of caspase-3 expression level between positive group with cinnamon extract group of 100 and 200mg/kgBW (p>0,05) and there were also no mean differences of positive group dopamine level with group of cinnamon extract of 100 and 200mg/kgBW (p>0.05). Conclussion Cinnamomum burmanii extract at dose of 100 and 200mg/kgBW were effective in the protection against neuronal cell death in haloperidol induced male Wistar white rats.

scholarly journals Role of oxidative stress and caspase 3 in CD47-mediated neuronal cell death

2009 ◽  
Vol 108 (2) ◽  
pp. 430-436 ◽  
Author(s):  
Changhong Xing ◽  
Sunryung Lee ◽  
Woo Jean Kim ◽  
Guang Jin ◽  
Yong-Guang Yang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell

Caspase-3-like proteases and 6-hydroxydopamine induced neuronal cell death

1999 ◽  
Vol 64 (1) ◽  
pp. 141-148 ◽  
Author(s):  
Richard C. Dodel ◽  
Yansheng Du ◽  
Kelly R. Bales ◽  
Zaodong Ling ◽  
Paul M. Carvey ◽  
...  
Keyword(s):  
Cell Death ◽  
Caspase 3 ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
6 Hydroxydopamine

scholarly journals Netrin-1 receptor UNC5C cleavage by active δ-secretase enhances neurodegeneration, promoting Alzheimer’s disease pathologies

2021 ◽  
Vol 7 (16) ◽  
pp. eabe4499
Author(s):  
Guiqin Chen ◽  
Seong Su Kang ◽  
Zhihao Wang ◽  
Eun Hee Ahn ◽  
Yiyuan Xia ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Cell Death ◽  
Axon Guidance ◽  
Neural Development ◽  
Caspase 3 ◽  
Late Onset ◽  
Neuronal Cell Death ◽  
Neuronal Cell ◽  
Cognitive Disorders

Netrin-1, a family member of laminin-related secreted proteins, mediates axon guidance and cell migration during neural development. T835M mutation in netrin receptor UNC5C predisposes to the late-onset Alzheimer’s disease (AD) and increases neuronal cell death. However, it remains unclear how this receptor is molecularly regulated in AD. Here, we show that δ-secretase selectively cleaves UNC5C and escalates its proapoptotic activity, facilitating neurodegeneration in AD. Netrin deficiency activates δ-secretase that specifically cuts UNC5C at N467 and N547 residues and enhances subsequent caspase-3 activation, additively augmenting neuronal cell death. Blockade of δ-secretase cleavage of UNC5C diminishes T835M mutant’s proapoptotic activity. Viral expression of δ-secretase–truncated UNC5C fragments into APP/PS1 mice strongly accelerates AD pathologies, impairing learning and memory. Conversely, deletion of UNC5C from netrin-1–depleted mice attenuates AD pathologies and rescues cognitive disorders. Hence, δ-secretase truncates UNC5C and elevates its neurotoxicity, contributing to AD pathogenesis.

Sign in / Sign up

Export Citation Format

Share Document