Trimethyltin initially activates the caspase 8/caspase 3 pathway for damaging the primary cultured cortical neurons derived from embryonic mice

2011 ◽  
Vol 89 (4) ◽  
pp. 552-561 ◽  
Author(s):  
Nobuyuki Kuramoto ◽  
Keiichi Seko ◽  
Chie Sugiyama ◽  
Makoto Shuto ◽  
Kiyokazu Ogita
Keyword(s):  
Cortical Neurons ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Cultured Cortical Neurons

scholarly journals Caspase-8 and Caspase-3 Are Expressed by Different Populations of Cortical Neurons Undergoing Delayed Cell Death after Focal Stroke in the Rat

1999 ◽  
Vol 19 (14) ◽  
pp. 5932-5941 ◽  
Author(s):  
James J. Velier ◽  
Julie A. Ellison ◽  
Kristine K. Kikly ◽  
Patricia A. Spera ◽  
Frank C. Barone ◽  
...  
Keyword(s):  
Cell Death ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Caspase 8 ◽  
Delayed Cell Death ◽  
Different Populations

scholarly journals Proteasome Inhibitors Induce Cytochrome c–Caspase-3-Like Protease-Mediated Apoptosis in Cultured Cortical Neurons

2000 ◽  
Vol 20 (1) ◽  
pp. 259-265 ◽  
Author(s):  
Jian Hua Qiu ◽  
Akio Asai ◽  
Shunji Chi ◽  
Nobuhito Saito ◽  
Hirofumi Hamada ◽  
...  
Keyword(s):  
Cytochrome C ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Proteasome Inhibitors ◽  
Cultured Cortical Neurons

scholarly journals Green Tea Polyphenols Attenuated Glutamate Excitotoxicity via Antioxidative and Antiapoptotic Pathway in the Primary Cultured Cortical Neurons

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Lin Cong ◽  
Chang Cao ◽  
Yong Cheng ◽  
Xiao-Yan Qin
Keyword(s):  
Green Tea ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
Neuroprotective Effect ◽  
Tea Polyphenols ◽  
Green Tea Polyphenols ◽  
Glutamate Excitotoxicity ◽  
Sod Activity ◽  
Antiapoptotic Proteins ◽  
Cultured Cortical Neurons

Green tea polyphenols are a natural product which has antioxidative and antiapoptotic effects. It has been shown that glutamate excitotoxicity induced oxidative stress is linked to neurodegenerative diseases such as Alzheimer’s disease and Parkinson’s disease. In this study we explored the neuroprotective effect of green teen polyphenols against glutamate excitotoxicity in the primary cultured cortical neurons. We found that green tea polyphenols protected against glutamate induced neurotoxicity in the cortical neurons as measured by MTT and TUNEL assays. Green tea polyphenols were then showed to inhibit the glutamate induced ROS release and SOD activity reduction in the neurons. Furthermore, our results demonstrated that green tea polyphenols restored the dysfunction of mitochondrial pro- or antiapoptotic proteins Bax, Bcl-2, and caspase-3 caused by glutamate. Interestingly, the neuroprotective effect of green tea polyphenols was abrogated when the neurons were incubated with siBcl-2. Taken together, these results demonstrated that green tea polyphenols protected against glutamate excitotoxicity through antioxidative and antiapoptotic pathways.

scholarly journals A role for c-Jun N-terminal kinase 1 (JNK1), but not JNK2, in the beta-amyloid-mediated stabilization of protein p53 and induction of the apoptotic cascade in cultured cortical neurons

2003 ◽  
Vol 371 (3) ◽  
pp. 789-798 ◽  
Author(s):  
Marie P. FOGARTY ◽  
Eric J. DOWNER ◽  
Veronica CAMPBELL
Keyword(s):  
Cell Death ◽  
Dna Fragmentation ◽  
Cortical Neurons ◽  
Caspase 3 ◽  
P53 Protein ◽  
Neuronal Cell ◽  
P53 Expression ◽  
Protein P53 ◽  
Cultured Cortical Neurons ◽  
Apoptotic Cascade

β-Amyloid (Aβ) peptide has been shown to induce neuronal apoptosis; however, the mechanisms underlying Aβ-induced neuronal cell death remain to be fully elucidated. The stress-activated protein kinase, c-Jun N-terminal kinase (JNK), is activated in response to cellular stress and has been identified as a proximal mediator of cell death. In the present study, expression of active JNK was increased in the nucleus and cytoplasm of Aβ-treated cells. Evaluation of the nature of the JNK isoforms activated by Aβ revealed a transient increase in JNK1 activity that reached its peak at 1 h and a later activation (at 24 h) of JNK2. The tumour suppressor protein, p53, is a substrate for JNK and can serve as a signalling molecule in apoptosis. In cultured cortical neurons, we found that Aβ increased p53 protein expression and phosphorylation of p53 at Ser15. Thus it appears that Aβ increases p53 expression via phosphorylation-mediated stabilization of the protein. Given the lack of availability of a JNK inhibitor that can distinguish between JNK1- and JNK2-mediated effects, we employed antisense technology to deplete cells of JNK1 or JNK2 selectively. Using this strategy, the respective roles of JNK1 and JNK2 on the Aβ-mediated activation of the apoptotic cascade (i.e. p53 stabilization, caspase 3 activation and DNA fragmentation) were examined. The results obtained demonstrate a role for JNK1 in the Aβ-induced stabilization of p53, activation of caspase 3 and DNA fragmentation. In contrast, depletion of JNK2 had no effect on the proclivity of Aβ to activate capase 3 or induce DNA fragmentation. These results demonstrate a significant role for JNK1 in Aβ-mediated induction of the apoptotic cascade in cultured cortical neurons.

scholarly journals The Bacterial Enzyme Cas13 Interferes with Neurite Outgrowth from Cultured Cortical Neurons

Toxins ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 262
Author(s):  
Qin-Wei Wu ◽  
Josef P. Kapfhammer
Keyword(s):  
Rna Editing ◽  
Cortical Neurons ◽  
High Efficiency ◽  
Primary Cultures ◽  
Cultured Neurons ◽  
Therapeutic Tool ◽  
Bacterial Enzyme ◽  
Rna Targeting ◽  
Cultured Cortical Neurons ◽  
New Generation

The CRISPR-Cas13 system based on a bacterial enzyme has been explored as a powerful new method for RNA manipulation. Due to the high efficiency and specificity of RNA editing/interference achieved by this system, it is currently being developed as a new therapeutic tool for the treatment of neurological and other diseases. However, the safety of this new generation of RNA therapies is still unclear. In this study, we constructed a vector expressing CRISPR-Cas13 under a constitutive neuron-specific promoter. CRISPR-Cas13 from Leptotrichia wadei was expressed in primary cultures of mouse cortical neurons. We found that the presence of CRISPR-Cas13 impedes the development of cultured neurons. These results show a neurotoxic action of Cas13 and call for more studies to test for and possibly mitigate the toxic effects of Cas13 enzymes in order to improve CRISPR-Cas13-based tools for RNA targeting.

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