Salubrinal protects against rotenone-induced SH-SY5Y cell death via ATF4-parkin pathway

Wu, Liang; Luo, Na; Zhao, Hongrui; Gao, Qing; Lu, Jie; Pan, Yang; Shi, Jingping; Tian, You‐Yong; Zhang, Yingdong

doi:10.1016/j.brainres.2014.01.003

Cited by 53 publications

(40 citation statements)

References 39 publications

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“…Enhancement of eIF2α phosphorylation results in a halt in protein synthesis, permitting cells to recover from consequences of endoplasmic reticulum (ER) stress that can otherwise lead to apoptosis [23]. Until now, the reported roles of salubrinal include acceleration of bone wounds healing in mice [24], stimulation of osteoblast differentiation [25,26], attenuation of nuclear factor κB-mediated molecular signals [27], protection against cell apoptosis [28,29], and so on. Recently, upregulation of phosp-eIF2α was found in TcdB-exposed CT26 cell line (BALB/C mouse colon tumor cells) [30] and in mice cecum and colon tissues receiving C. difficile VPI10463 vegetative cells [31], which seemed to protect host cells and animals.…”

Section: Introductionmentioning

confidence: 99%

Salubrinal protects against toxin B-induced CT26 cell death

Chen

Sun

et al. 2017

ABBS

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Clostridium difficile (C. difficile) is considered to be the major cause of the antibiotic-associated diarrhea and pseudomembranous colitis in animals and humans. The prevalence of C. difficile infections (CDI) has been increasing since 2000. Two exotoxins of C. difficile, Toxin A (TcdA) and Toxin B (TcdB), are the main virulence factors of CDI, which can induce glucosylation of Rho GTPases in host cytosol, leading to cell morphological changes, cell apoptosis, and cell death. The mechanism of TcdB-induced cell death has been investigated for decades, but it is still not completely understood. It has been reported that TcdB induces endoplasmic reticulum stress via PERK-eIF2α signaling pathway in CT26 cell line (BALB/C mouse colon tumor cells). In this study, we found that salubrinal, a selective inhibitor of eIF2α dephosphorylation, efficiently protects CT26 cell line against TcdB-induced cell death and tried to explore the mechanism underlying in this protective effect. Our results demonstrated that salubrinal protects CT26 cells from TcdB-mediated cytotoxic and cytopathic effect, inhibits apoptosis and death of the toxin-exposed cells via caspase-9-dependent pathway, eIF2α signaling pathway, and autophagy. These findings will be helpful for the development of CDI therapies.

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Section: Introductionmentioning

confidence: 99%

Salubrinal protects against toxin B-induced CT26 cell death

Chen

Sun

et al. 2017

ABBS

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“…It was also identified that the ER stress‐induced activation of the transcription factor ATF‐4 was required for miR‐29a expression. PERK activation and ATF4 signalling have been described as regulators of neurodegeneration and ER stress‐induced apoptosis in disease models of Alzheimer's disease (Devi & Ohno, ), Parkinson's disease (Wu et al ., ) and amyotrophic lateral sclerosis (Matus et al ., ), suggesting that inhibition of miR‐29a could represent a novel therapeutic target for neurodegenerative disorders. ATF4 has previously been demonstrated to be an important ‘switch’ in ER stress‐induced activation of apoptosis by upregulating the expression of puma (Galehdar et al ., ).…”

Section: Discussionmentioning

confidence: 99%

Endoplasmic reticulum stress‐mediated upregulation of miR‐29a enhances sensitivity to neuronal apoptosis

Nolan

Walter

Tuffy

et al. 2016

Eur J of Neuroscience

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“…However, derivatives exhibiting improvedproperties are devoid of cinnamoyl moiety. [73,75] However,o ther cell types might reactd ifferently upon treatment with salubrinal. Inhibitors of eIF2a dephosphorylation and their cytoprotective activity Ac innamamide derivative, salubrinal (35), prevented dephosphorylation of eukaryotic translation initiation factor 2s ubunit a (eIF2a)byinhibiting the formation of the GADD34/PP1 protein complex.…”

Section: G-secretase Inhibitorsmentioning

confidence: 99%

“…The positive impact of salubrinal on neuronal cells was shown in severals tudies, and its potential use in AD and PD has been suggested. [73,75] However,o ther cell types might reactd ifferently upon treatment with salubrinal. For instance, it caused pancreatic andE pstein-Barr virus (EBV)-transformed Bcell apopto-sis, as well as enhanced cisplatin-induced nephrotoxicity.…”

Section: Inhibitors Of Eif2a Dephosphorylation and Their Cytoprotectimentioning

confidence: 99%

Cinnamamide Derivatives for Central and Peripheral Nervous System Disorders—A Review of Structure–Activity Relationships

et al. 2015

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The cinnamamide scaffold has been incorporated in to the structure of numerous organic compounds with therapeutic potential. The scaffold enables multiple interactions, such as hydrophobic, dipolar, and hydrogen bonding, with important molecular targets. Additionally, the scaffold has multiple substitution options providing the opportunity to optimize and modify the pharmacological activity of the derivatives. In particular, cinnamamide derivatives have exhibited therapeutic potential in animal models of both central and peripheral nervous system disorders. Some have undergone clinical trials and were introduced on to the pharmaceutical market. The diverse activities observed in the nervous system included anticonvulsant, antidepressant, neuroprotective, analgesic, anti-inflammatory, muscle relaxant, and sedative properties. Over the last decade, research has focused on the molecular mechanisms of action of these derivatives, and the data reported in the literature include targeting the γ-aminobutyric acid type A (GABAA ) receptors, N-methyl-D-aspartate (NMDA) receptors, transient receptor potential (TRP) cation channels, voltage-gated potassium channels, histone deacetylases (HDACs), prostanoid receptors, opioid receptors, and histamine H3 receptors. Here, the literature data from reports evaluating cinnamic acid amide derivatives for activity in target-based or phenotypic assays, both in vivo and in vitro, relevant to disorders of the central and peripheral nervous systems are analyzed and structure-activity relationships discussed.

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Salubrinal protects against rotenone-induced SH-SY5Y cell death via ATF4-parkin pathway

Cited by 53 publications

References 39 publications

Salubrinal protects against toxin B-induced CT26 cell death

Salubrinal protects against toxin B-induced CT26 cell death

Endoplasmic reticulum stress‐mediated upregulation of miR‐29a enhances sensitivity to neuronal apoptosis

Cinnamamide Derivatives for Central and Peripheral Nervous System Disorders—A Review of Structure–Activity Relationships

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