Amyloid-β1-42 Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in U87 and SH-SY5Y Cells

Wang, Hongmei; Ma, Jianfang; Tan, Yuyan; Wang, Zhiquan; Chen, Sheng Di; Chen, Shengdi; Ding, Jianqing

doi:10.3233/jad-2010-091207

Cited by 78 publications

(38 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4,40 For instance, neurodegeneration after brain injury could be prevented by conditional Atg7 deficiency in mice, 48 and Beclin-1 silencing or chemical inhibition of autophagy protected from cell death in cell culture models of AD. 49 Similarly, pharmacological induction of autophagy via rapamycin turned out to be neurotoxic in alternative scenarios than those where protection was observed. 50,51 These data indicate that a tightly controlled balance of autophagic processes is mandatory for neuronal survival.…”

Section: Discussionmentioning

confidence: 99%

Spermidine protects against α-synuclein neurotoxicity

et al. 2014

View full text Add to dashboard Cite

These authors contributed equally to this work.Keywords: autophagy, aging, a-synuclein, dopaminergic neuron loss, motor dysfunction, neurodegeneration, Parkinson's disease, SpermidineAs our society ages, neurodegenerative disorders like Parkinson`s disease (PD) are increasing in pandemic proportions. While mechanistic understanding of PD is advancing, a treatment with well tolerable drugs is still elusive. Here, we show that administration of the naturally occurring polyamine spermidine, which declines continuously during aging in various species, alleviates a series of PD-related degenerative processes in the fruit fly Drosophila melanogaster and the nematode Caenorhabditis elegans, two established model systems for PD pathology. In the fruit fly, simple feeding with spermidine inhibited loss of climbing activity and early organismal death upon heterologous expression of human a-synuclein, which is thought to be the principal toxic trigger of PD. In this line, administration of spermidine rescued a-synuclein-induced loss of dopaminergic neurons, a hallmark of PD, in nematodes. Alleviation of PD-related neurodegeneration by spermidine was accompanied by induction of autophagy, suggesting that this cytoprotective process may be responsible for the beneficial effects of spermidine administration.

show abstract

Section: Discussionmentioning

confidence: 99%

Spermidine protects against α-synuclein neurotoxicity

et al. 2014

View full text Add to dashboard Cite

show abstract

“…Further, bufalin-induced autophagy was attenuated by an ROS scavenger (336). Some other cancer types for which ROS have been shown to effectively induce autophagic cell death are breast cancer (281), nonsmall cell lung cancer (NSCLC) (184), glioma (239,317), neuroblastoma (317), glioblastoma (53), and cervical cancer (53, 108).…”

Section: Ros and Autophagymentioning

confidence: 99%

Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy

Gupta

Hevia

Patchva

et al. 2012

Antioxidants & Redox Signaling

607

464

View full text Add to dashboard Cite

Significance: Extensive research during the last quarter century has revealed that reactive oxygen species (ROS) produced in the body, primarily by the mitochondria, play a major role in various cell-signaling pathways. Most risk factors associated with chronic diseases (e.g., cancer), such as stress, tobacco, environmental pollutants, radiation, viral infection, diet, and bacterial infection, interact with cells through the generation of ROS. Recent Advances: ROS, in turn, activate various transcription factors (e.g., nuclear factor kappa-light-chain-enhancer of activated B cells [NF-jB], activator protein-1, hypoxia-inducible factor-1a, and signal transducer and activator of transcription 3), resulting in the expression of proteins that control inflammation, cellular transformation, tumor cell survival, tumor cell proliferation and invasion, angiogenesis, and metastasis. Paradoxically, ROS also control the expression of various tumor suppressor genes (p53, Rb, and PTEN). Similarly, c-radiation and various chemotherapeutic agents used to treat cancer mediate their effects through the production of ROS. Interestingly, ROS have also been implicated in the chemopreventive and anti-tumor action of nutraceuticals derived from fruits, vegetables, spices, and other natural products used in traditional medicine. Critical Issues: These statements suggest both ''upside'' (cancer-suppressing) and ''downside'' (cancer-promoting) actions of the ROS. Thus, similar to tumor necrosis factor-a, inflammation, and NF-jB, ROS act as a double-edged sword. This paradox provides a great challenge for researchers whose aim is to exploit ROS stress for the development of cancer therapies. Future Directions: The various mechanisms by which ROS mediate paradoxical effects are discussed in this article. The outstanding questions and future directions raised by our current understanding are discussed. Antioxid. Redox Signal. 16, 1295Signal. 16, -1322

show abstract

“…The viability of the astrocytes was evaluated by MTT assay as previously described [5]. In brief, the cells were treated with NBP for 24 h. MTT (0.5 mg/ml) was added to the medium and incubated for an additional 4 h. At the end of the incubation period, the medium with MTT was removed, and 100 µl DMSO was subsequently added to each well.…”

Section: Methodsmentioning

confidence: 99%

3-N-Butylphthalide (NBP) Attenuates the Amyloid-�-Induced Inflammatory Responses in Cultured Astrocytes via the Nuclear Factor-κB Signaling Pathway

Wang

Zhang

Huang

et al. 2013

Cell Physiol Biochem

View full text Add to dashboard Cite

Background/Aims: Activation of astrocytes is a common feature of Alzheimer's disease (AD). Proinflammatory molecules produced by activated astrocytes contribute to neuronal damage in AD. Moreover, dl-3-n-butylphthalide (NBP) has been reported to attenuate astroglial activation and exert neuroprotective effects in AD transgenic mice. However, the mechanism by which NBP inhibits activated astrocytes is poorly understood. Methods: In this study, the primary astrocytes were obtained from the cerebral cortices of 1-day-old Sprague-Dawley rats. The levels of GFAP, COX-2, NF-κB, and IκBa were examined by Western blotting and the levels of TNF-a and IL-6 were determined by ELISA. Results: NBP inhibited the amyloid-ß (Aß)-induced activation of astrocytes and the up-regulation of proinflammatory molecules. Importantly, NBP markedly suppressed Aß-induced IκBa degradation and nuclear factor-κB (NF-κB) translocation. Conclusion: Our results suggest that NBP attenuates Aß-induced activation of astrocytes and neuroinflammation via inhibition of the NF-κB signaling pathway.

show abstract

Amyloid-β1-42 Induces Reactive Oxygen Species-Mediated Autophagic Cell Death in U87 and SH-SY5Y Cells

Cited by 78 publications

References 0 publications

Spermidine protects against α-synuclein neurotoxicity

Spermidine protects against α-synuclein neurotoxicity

Upsides and Downsides of Reactive Oxygen Species for Cancer: The Roles of Reactive Oxygen Species in Tumorigenesis, Prevention, and Therapy

3-N-Butylphthalide (NBP) Attenuates the Amyloid-�-Induced Inflammatory Responses in Cultured Astrocytes via the Nuclear Factor-κB Signaling Pathway

Contact Info

Product

Resources

About