Tubuloside B fromCistanche salsaRescues the PC12 Neuronal Cells from 1-Methyl-4-phenylpyridinium Ion-Induced Apoptosis and Oxidative Stress

Planta Medica ◽  
2002 ◽  
Vol 68 (11) ◽  
pp. 966-970 ◽  
Author(s):  
Guoqing Sheng ◽  
Xiaoping Pu ◽  
Li Lei ◽  
Pengfei Tu ◽  
Changling Li
Keyword(s):  
Oxidative Stress ◽  
Neuronal Cells ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Pink1 attenuates propofol-induced apoptosis and oxidative stress in developing neurons

2017 ◽  
Vol 32 (1) ◽  
pp. 62-69 ◽  
Author(s):  
Chao Liang ◽  
Fang Du ◽  
Jing Cang ◽  
Zhanggang Xue
Keyword(s):  
Oxidative Stress ◽  
Induced Apoptosis ◽  
Developing Neurons ◽  
And Oxidative Stress

Correction of ATM mutations in iPS cells from two ataxia-telangiectasia patients restores DNA damage and oxidative stress responses

2020 ◽  
Vol 29 (6) ◽  
pp. 990-1001 ◽  
Author(s):  
Dmitry A Ovchinnikov ◽  
Sarah L Withey ◽  
Hannah C Leeson ◽  
U Wang Lei ◽  
Ashmitha Sundarrajan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dna Damage ◽  
Stress Responses ◽  
Ataxia Telangiectasia ◽  
Compound Heterozygous ◽  
Gene Correction ◽  
Atm Kinase ◽  
Atm Protein ◽  
Induced Apoptosis ◽  
And Oxidative Stress

Abstract Patients with ataxia-telangiectasia (A-T) lack a functional ATM kinase protein and exhibit defective repair of DNA double-stranded breaks and response to oxidative stress. We show that CRISPR/Cas9-assisted gene correction combined with piggyBac (PB) transposon-mediated excision of the selection cassette enables seamless restoration of functional ATM alleles in induced pluripotent stem cells from an A-T patient carrying compound heterozygous exonic missense/frameshift mutations, and from a patient with a homozygous splicing acceptor mutation of an internal coding exon. We show that the correction of one allele restores expression of ~ 50% of full-length ATM protein and ameliorates DNA damage-induced activation (auto-phosphorylation) of ATM and phosphorylation of its downstream targets, KAP-1 and H2AX. Restoration of ATM function also normalizes radiosensitivity, mitochondrial ROS production and oxidative-stress-induced apoptosis levels in A-T iPSC lines, demonstrating that restoration of a single ATM allele is sufficient to rescue key ATM functions. Our data further show that despite the absence of a functional ATM kinase, homology-directed repair and seamless correction of a pathogenic ATM mutation is possible. The isogenic pairs of A-T and gene-corrected iPSCs described here constitute valuable tools for elucidating the role of ATM in ageing and A-T pathogenesis.

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