Role of increased expression of the proteasome in the protective effects of sulforaphane against hydrogen peroxide-mediated cytotoxicity in murine neuroblastoma cells

Kwak, Mi Kyung; Cho, Jeong Min; Huang, Bo; Shin, Soona; Kensler, Thomas W.

doi:10.1016/j.freeradbiomed.2007.05.029

Cited by 132 publications

(109 citation statements)

References 38 publications

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“…In addition, the up-regulation of Psmd13, GRP78/Hspa5 and Pdia3 also responded to the cell stress. Psmd13 could be induced in multiple tissues of mouse including brain by exogenous chemical treatment and has a role in degradation of abnormal protein [59]. Pdia3 can act as molecular chaperones by inhibiting the aggregation of unfolded/misfolded proteins at the ER.…”

Section: Discussionmentioning

confidence: 99%

A proteomic analysis of prenatal transfer of microcystin-LR induced neurotoxicity in rat offspring

Zhao

Chen

2015

Journal of Proteomics

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Section: Discussionmentioning

confidence: 99%

A proteomic analysis of prenatal transfer of microcystin-LR induced neurotoxicity in rat offspring

Zhao

Chen

2015

Journal of Proteomics

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“…Next, as an independent test, we examined bbs4 morphants coinjected with SFN, a known transcriptional activator of proteasomal subunits (36). Upon blind scoring at the 9 ± 1 ss, there was a significant reduction of bbs4 morphants with CE and somitic defects (P < 0.001; Figure 5B).…”

Section: [Rpn10]mentioning

confidence: 99%

Ciliopathy proteins regulate paracrine signaling by modulating proteasomal degradation of mediators

et al. 2014

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Cilia are critical mediators of paracrine signaling; however, it is unknown whether proteins that contribute to ciliopathies converge on multiple paracrine pathways through a common mechanism. Here, we show that loss of cilopathy-associated proteins Bardet-Biedl syndrome 4 (BBS4) or oral-facial-digital syndrome 1 (OFD1) results in the accumulation of signaling mediators normally targeted for proteasomal degradation. In WT cells, several BBS proteins and OFD1 interacted with proteasomal subunits, and loss of either BBS4 or OFD1 led to depletion of multiple subunits from the centrosomal proteasome. Furthermore, overexpression of proteasomal regulatory components or treatment with proteasomal activators sulforaphane (SFN) and mevalonolactone (MVA) ameliorated signaling defects in cells lacking BBS1, BBS4, and OFD1, in morphant zebrafish embryos, and in induced neurons from Ofd1-deficient mice. Finally, we tested the hypothesis that other proteasome-dependent pathways not known to be associated with ciliopathies are defective in the absence of ciliopathy proteins. We found that loss of BBS1, BBS4, or OFD1 led to decreased NF-κB activity and concomitant IκBβ accumulation and that these defects were ameliorated with SFN treatment. Taken together, our data indicate that basal body proteasomal regulation governs paracrine signaling pathways and suggest that augmenting proteasomal function might benefit ciliopathy patients.

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“…1C). Kwak et al (2007) The oak extract-pretreated groups exhibited decreased H 2 O 2 -induced cytotoxicity and apoptotic cell death in a dose-dependent manner.…”

Section: Resultsmentioning

confidence: 89%

Anti-apoptotic Effect of Steam Exploded Quercus variabilis

Jo¹,

Jung²,

Nam³

et al. 2015

Journal of the Korean Wood Science and Technology

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We hypothesized that the extract from steam exploded Q. variabilis might be cytoprotective for tenofibroblasts cells during oxidative stress. In the present study, the extracts obtained from steam exploded (severity log Ro 4.68) Q. variabilis contained high quantities of phenolics and flavonoids contents. Also, the extracts appear to have, on these tenofibroblasts, a protective effect against oxidative stress. Tenofibroblasts cells incubated with the extracts and stressed with H2O2 showed an increase in cell viability by MTT assay. The extracts is found to inhibit H2O2-induced apoptosis in tenofibroblasts cells, as shown by Annexin V/PI double staining analysis. Western blot data showed that in the extracts/H2O2-treated cells, the extracts inhibited the H2O2-dependent phosphorylation of ERK and p38. From these results, it is suggested that the extracts showed the protective effect on H2O2-mediated oxidative stress. The main chemical compounds of the extract was identified as 1,8-cineole by GC-MS analysis. The anti-apoptosis activity is accordingly believed to be attributable to the 1,8-cineole.

show abstract

Role of increased expression of the proteasome in the protective effects of sulforaphane against hydrogen peroxide-mediated cytotoxicity in murine neuroblastoma cells

Cited by 132 publications

References 38 publications

A proteomic analysis of prenatal transfer of microcystin-LR induced neurotoxicity in rat offspring

A proteomic analysis of prenatal transfer of microcystin-LR induced neurotoxicity in rat offspring

Ciliopathy proteins regulate paracrine signaling by modulating proteasomal degradation of mediators

Anti-apoptotic Effect of Steam Exploded Quercus variabilis

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