Emerging roles of the γ-secretase-notch axis in inflammation

Cheng, Yuxiang; Choi, Yong-Sung; Sobey, Christopher G.; Arumugam, Thiruma V.; Jo, Dong Gyu

doi:10.1016/j.pharmthera.2014.11.005

Cited by 23 publications

(19 citation statements)

References 128 publications

(168 reference statements)

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“…Growing evidence shows that Notch signaling plays a crucial role in the pathogenesis of multiple inflammatory diseases[16,17]. Our findings of increased activation of Notch signaling are consistent with ConA-induced liver fibrosis.…”

Section: Discussionsupporting

confidence: 89%

Notch signaling mediated by TGF-β/Smad pathway in concanavalin A-induced liver fibrosis in rats

Wang

Shen

Han

et al. 2017

WJG

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AIMTo explore the exact interaction between Notch and transforming growth factor (TGF)-β signaling in liver fibrosis.METHODSWe established a rat model of liver fibrosis induced by concanavalin A. Peripheral blood mononuclear cells (PBMCs) were isolated from the modeled rats, and cultured with γ-secretase inhibitor DAPT and TGF-β inhibitor for 24 h. The mRNA levels of Notch and TGF-β signaling were detected by quantitative real-time polymerase chain reaction. Expression of Notch and TGF-β proteins was analyzed by western blotting.RESULTSCompared to control rats, Notch and TGF-β signaling was activated in PBMCs of model rats. Administration of DAPT and TGF-β inhibitor suppressed Notch and TGF-β signal transducer in PBMCs of model rats. DAPT reduced mRNA and protein expression of TGF-β signaling, such as TGF-β1 and Smad3. TGF-β inhibitor also downregulated Notch1, Hes1 and Hes5, and mRNA and protein expression of the Notch signaling pathway.CONCLUSIONNotch and TGF-β signaling play a role in liver fibrosis. TGF-β signaling upregulates Notch signaling, which promotes TGF-β signaling.

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Section: Discussionsupporting

confidence: 89%

Notch signaling mediated by TGF-β/Smad pathway in concanavalin A-induced liver fibrosis in rats

Wang

Shen

Han

et al. 2017

WJG

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“…ACCEPTED MANUSCRIPT 8 Remaining DNA and impurities on the membrane are washed away by wash buffers. At last, pure RNA is eluted by nuclease-free water.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

“…In addition, increasing evidence has shown that Notch plays important roles in the regulation of inflammatory responses in many diseases including cardiovascular disease, multiple sclerosis, asthma, stroke, Alzheimer's disease, and rheumatoid arthritis [7][8][9]. The expression of Notch in RA synoviocytes is shown to contribute to TNFα-induced proliferation, whereas Jagged-1, one of Notch ligands, suppresses collagen-induced arthritis (CIA) progression by inhibiting CD8 + T cell response [10].…”

Section: Introductionmentioning

confidence: 99%

Notch1 targeting siRNA delivery nanoparticles for rheumatoid arthritis therapy

Kim

Park

Lee

et al. 2015

Journal of Controlled Release

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“…(E) (Kumar et al, 2012 ; Brune et al, 2013 ; Ruiz et al, 2013 ; Sandberg et al, 2013 ; Bakunina et al, 2015 ; Zhao et al, 2015 ). (F) (Hoyne et al, 2001 ; Arumugam et al, 2006 ; Fung et al, 2007 ; Fernandez et al, 2008 ; Palaga et al, 2008 ; Ito et al, 2012 ; Wongchana and Palaga, 2012 ; Zhang et al, 2012 ; Radtke et al, 2013 ; Yao et al, 2013b ; Cheng et al, 2015 ). (G) (O’Dea and Hoffmann, 2009 ; Crampton and O’keeffe, 2013 ; Snow et al, 2014 ).…”

Section: Part 2 Molecular Consequences Of Exposure To Inflammatory Sunclassified

Systems approach to the study of brain damage in the very preterm newborn

Leviton

Gressèns

Dammann

2015

Front. Syst. Neurosci.

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Background: A systems approach to the study of brain damage in very preterm newborns has been lacking.Methods: In this perspective piece, we offer encephalopathy of prematurity as an example of the complexity and interrelatedness of brain-damaging molecular processes that can be initiated inflammatory phenomena.Results: Using three transcription factors, nuclear factor-kappa B (NF-κB), Notch-1, and nuclear factor erythroid 2 related factor 2 (NRF2), we show the inter-connectedness of signaling pathways activated by some antecedents of encephalopathy of prematurity.Conclusions: We hope that as biomarkers of exposures and processes leading to brain damage in the most immature newborns become more readily available, those who apply a systems approach to the study of neuroscience can be persuaded to study the pathogenesis of brain disorders in the very preterm newborn.

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Emerging roles of the γ-secretase-notch axis in inflammation

Cited by 23 publications

References 128 publications

Notch signaling mediated by TGF-β/Smad pathway in concanavalin A-induced liver fibrosis in rats

Notch signaling mediated by TGF-β/Smad pathway in concanavalin A-induced liver fibrosis in rats

Notch1 targeting siRNA delivery nanoparticles for rheumatoid arthritis therapy

Systems approach to the study of brain damage in the very preterm newborn

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