Rb-mediated apoptosis or proliferation: It's up to JNK

Mollereau, Bertrand; Ma, Dandan

doi:10.1080/15384101.2015.1119492

Cited by 10 publications

(8 citation statements)

References 7 publications

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“…The JNK pathway is activated in response to various stimuli, such as infection, inflammation, oxidative stress, DNA damage, osmotic stress or cytoskeletal changes, and plays evolutionarily conserved roles in numerous immune responses 34 . Earlier analyses of JNK-regulated pathways have revealed crucial roles in both cell proliferation and death 35 , 36 . Since JNK is a key component of innate immunity, bacteria, viruses and eukaryotic parasites can directly “tamper with” this pathway to evade or suppress immune responses 37 – 39 .…”

Section: Discussionmentioning

confidence: 99%

HEV ORF3 downregulates TLR7 to inhibit the generation of type I interferon via impairment of multiple signaling pathways

Lei

Zhang

et al. 2018

Sci Rep

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Hepatitis E is the most common type of acute hepatitis prevalent worldwide. The open reading frame 3 protein of HEV (HEV ORF3) is proposed to create a favorable environment for viral replication and pathogenesis. However, the mechanisms by which HEV overcomes the effects of host immunity, particularly the role of ORF3, remain to be established. Expression of IFNα and IFNβ in supernatant and cell samples was examined via ELISA and quantitative RT-PCR. The protein levels of specific signaling factors in cells overexpressing HEV ORF3 were examined via western blot. Analyses of cells transfected with vectors expressing ORF3 demonstrated that HEV ORF3 significantly impairs the generation of endogenous type I interferon through downregulating TLR3 and TLR7 as well as their corresponding downstream signaling pathways. Moreover, inhibition of NFκB, JAK/STAT and JNK/MAPK signaling pathways contributed significantly to suppression of increased levels of TLR7. Levels of p-P65, p-STAT1 and p-JNK were markedly impaired in ORF3-expressing cells, even upon treatment with the respective agonists. HEV ORF3 inhibits the production of endogenous type I interferon through downregulation of TLR3 and TLR7. Furthermore, suppression of TLR7 is achieved through impairment of multiple signaling pathways, including NFκB, JAK/STAT and JNK/MAPK.

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Section: Discussionmentioning

confidence: 99%

HEV ORF3 downregulates TLR7 to inhibit the generation of type I interferon via impairment of multiple signaling pathways

Lei

Zhang

et al. 2018

Sci Rep

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“…The JNK and Wnt/β-catenin pathways act as critical intermediates and convergence points in immune system signaling ( 27 , 28 ). These two signaling pathways can also regulate cell proliferation and apoptosis ( 29 – 31 ). It is widely accepted that JNK and Wnt/β-catenin signaling pathways can be activated by TNF-α treatment ( 32 ).…”

Section: Discussionmentioning

confidence: 99%

miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1

Chen

Zhang

et al. 2018

Braz J Med Biol Res

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MicroRNAs (miRNAs) have been reported to be associated with heart valve disease, which can be caused by inflammation. This study aimed to investigate the functional impacts of miR-27a on TNF-α-induced inflammatory injury in human mitral valve interstitial cells (hMVICs). hMVICs were subjected to 40 ng/mL TNF-α for 48 h, before which the expressions of miR-27a and NELL-1 in hMVICs were altered by stable transfection. Trypan blue staining, BrdU incorporation assay, flow cytometry detection, ELISA, and western blot assay were performed to detect cell proliferation, apoptosis, and the release of proinflammatory cytokines. We found that miR-27a was lowly expressed in response to TNF-α exposure in hMVICs. Overexpression of miR-27a rescued hMVICs from TNF-α-induced inflammatory injury, as cell viability and BrdU incorporation were increased, apoptotic cell rate was decreased, Bcl-2 was up-regulated, Bax and cleaved caspase-3/9 were down-regulated, and the release of IL-1β, IL-6, and MMP-9 were reduced. NELL-1 was positively regulated by miR-27a, and NELL-1 up-regulation exhibited protective functions during TNF-α-induced cell damage. Furthermore, miR-27a blocked JNK and Wnt/β-catenin signaling pathways, and the blockage was abolished when NELL-1 was silenced. This study demonstrated that miR-27a overexpression protected hMVICs from TNF-α-induced cell damage, which might be via up-regulation of NELL-1 and thus modulation of JNK and Wnt/β-catenin signaling pathways.

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“…Unlike loss of other genes well known to participate in spindle assembly and orientation ( Nakajima et al , 2013 ; Poulton et al , 2014 ), Shot loss does not appear to significantly up-regulate p-JNK levels, suggesting apoptosis is induced through an alternative pathway ( Figure 7 ). Although JNK signaling has a clear canonical role in apoptosis, alternative pathways likely play a role in apoptotic induction ( Strasser et al , 2000 ), and furthermore, JNK signaling has been shown to play an activating role in cell proliferation under certain conditions such as compensatory growth ( Mollereau and Ma, 2016 ).…”

Section: Discussionmentioning

confidence: 99%

Diverse mitotic functions of the cytoskeletal cross-linking protein Shortstop suggest a role in Dynein/Dynactin activity

Dewey

Johnston

2017

MBoC

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Rb-mediated apoptosis or proliferation: It's up to JNK

Cited by 10 publications

References 7 publications

HEV ORF3 downregulates TLR7 to inhibit the generation of type I interferon via impairment of multiple signaling pathways

HEV ORF3 downregulates TLR7 to inhibit the generation of type I interferon via impairment of multiple signaling pathways

miR-27a protects human mitral valve interstitial cell from TNF-α-induced inflammatory injury via up-regulation of NELL-1

Diverse mitotic functions of the cytoskeletal cross-linking protein Shortstop suggest a role in Dynein/Dynactin activity

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