Loss of ATM Impairs Proliferation of Neural Stem Cells Through Oxidative Stress-Mediated p38 MAPK Signaling

Stem Cells ◽  
2009 ◽  
Vol 27 (8) ◽  
pp. 1987-1998 ◽  
Author(s):  
Jeesun Kim ◽  
Paul K.Y. Wong
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
P38 Mapk ◽  
Mapk Signaling

Neuroprotective effects of amlodipine besylate and benidipine hydrochloride on oxidative stress-injured neural stem cells

2014 ◽  
Vol 1551 ◽  
pp. 1-12 ◽  
Author(s):  
Na-Young Choi ◽  
Hojin Choi ◽  
Hyun-Hee Park ◽  
Eun-Hye Lee ◽  
Hyun-Jeung Yu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Amlodipine Besylate ◽  
Neuroprotective Effects

scholarly journals Dual Specificity Phosphatase 6 Protects Neural Stem Cells from β-Amyloid-Induced Cytotoxicity through ERK1/2 Inactivation

Biomolecules ◽  
2018 ◽  
Vol 8 (4) ◽  
pp. 181 ◽  
Author(s):  
Wang Liao ◽  
Yuqiu Zheng ◽  
Wenli Fang ◽  
Shaowei Liao ◽  
Ying Xiong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Western Blot ◽  
Mitochondrial Dysfunction ◽  
Neuroprotective Effect ◽  
Dependent Manner ◽  
Dual Specificity Phosphatase ◽  
Cell Vitality ◽  
Dual Specificity

Alzheimer’s disease (AD) is a devastating neurodegenerative disease with limited treatment options and no cure. Beta-amyloid (Aβ) is a hallmark of AD that has potent neurotoxicity in neural stem cells (NSCs). Dual specificity phosphatase 6 (DUSP6) is a member of the mitogen-activated protein kinases (MAPKs), which is involved in regulating various physiological and pathological processes. Whether DUSP6 has a protective effect on Aβ-induced NSC injury remains to be explored. C17.2 neural stem cells were transfected with DUSP6-overexpressed plasmid. NSCs with or without DUSP6 overexpression were administrated with Aβ25–35 at various concentrations (i.e., 0, 2.5, 5 μM). DUSP6 expression after Aβ treatment was detected by Real-Time Polymerase Chain Reaction (RT-PCR) and Western blot and cell vitality was examined by the CCK8 assay. The oxidative stress (intracellular reactive oxygen species (ROS) and malondialdehyde (MDA)), endoplasmic reticulum stress (ER calcium level) and mitochondrial dysfunction (cytochrome c homeostasis) were tested. The expression of p-ERK1/2 and ERK1/2 were assayed by Western blot. Our results showed that Aβ decreased the expression of DUSP6 in a dose-dependent manner. The overexpression of DUSP6 increased the cell vitality of NSCs after Aβ treatment. Oxidative stress, ER stress, and mitochondrial dysfunction induced by Aβ could be restored by DUSP6 overexpression. Additionally, the Aβ-induced ERK1/2 activation was reversed. In summary, DUSP6 might have a neuroprotective effect on Aβ-induced cytotoxicity, probably via ERK1/2 activation.

scholarly journals Microarray Analyses Support a Role for Nurr1 in Resistance to Oxidative Stress and Neuronal Differentiation in Neural Stem Cells

Stem Cells ◽  
2007 ◽  
Vol 25 (2) ◽  
pp. 511-519 ◽  
Author(s):  
Kyle M. Sousa ◽  
Helena Mira ◽  
Anita C. Hall ◽  
Lottie Jansson-Sjöstrand ◽  
Moriaki Kusakabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Stem Cells ◽  
Neural Stem Cells ◽  
Neuronal Differentiation ◽  
Microarray Analyses

scholarly journals Protective Effect of Penetratin Analogue-Tagged SOD1 on Cisplatin-Induced Nephrotoxicity through Inhibiting Oxidative Stress and JNK/p38 MAPK Signaling Pathway

2021 ◽  
Vol 2021 ◽  
pp. 1-13
Author(s):  
Xiao-lu Wang ◽  
Liang Wang ◽  
Fo-lan Lin ◽  
Si-si Li ◽  
Ting-xuan Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Membrane ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Cell Apoptosis ◽  
Mapk Signaling ◽  
Tunel Assay ◽  
Mapk Signaling Pathway ◽  
Mapk Activation ◽  
Urea Nitrogen

Copper/zinc superoxide dismutase (SOD1) can clear cisplatin- (CP-) induced excessive reactive oxygen species (ROS), but exogenous SOD1 cannot enter cells because of its low biomembrane permeability. Cell-penetrating peptides (CPPs) can rapidly cross plasma membranes. This study is aimed at identifying an efficient and stable CPP-SOD1 and investigating its effects on CP-induced nephrotoxicity. We recombined SOD1 with 14 different CPPs and purified them using an NTA-Ni2+ column. In in vitro experiments, CPPs-SOD1 cell membrane penetration ability and JNK/p38 MAPK signaling pathway were evaluated using Western blotting. ROS production, mitochondrial membrane potential (MMP), and cell apoptosis were determined using flow cytometry and immunofluorescence staining in VERO and HK-2 cells. For in vivo experiments, mice were administered PSF-SOD1 for 2 h before cotreatment with a single CP injection for an additional 4 days. Blood and kidney samples were collected for renal function assessment (creatinine, urea nitrogen, histopathology, TUNEL assay, and JNK/p38 MAPK signaling pathway). Compared with TAT-SOD1, we found that PSF-SOD1 is more efficient at crossing the cell membrane and is stable after transduction into cells. Pretreatment with PSF-SOD1 inhibited CP-induced apoptosis, ROS generation, and JNK/p38 MAPK activation and restored CP-induced MMP loss in VERO and HK-2 kidney cells. Treatment of mice with PSF-SOD1 inhibited CP-induced serum creatinine, blood urea nitrogen elevation, and JNK/p38 MAPK activation. H&E staining and TUNEL assay indicated that kidney tissue damage was alleviated following PSF-SOD1 pretreatment. Overall, PSF-SOD1 ameliorated CP-induced renal damage by partially reducing oxidative stress and cell apoptosis by regulating JNK/p38 MAPK signaling pathway and might be a better cytoprotective agent than TAT-SOD1.

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