Sulforaphane induces autophagy through ERK activation in neuronal cells
Jo C, Kim S, Cho SJ, Choi KJ, Yun SM, Koh YH, Johnson GV, Park SI
FEBS letters · 52 citations
Review labels
Neutral facts our review recorded about how this study was done. They describe method, never whether we like the result.
How it was studied
- Design
- In vitro/mechanistic study (classified by our AI screen)
- Studied in
- Cells or lab samples
- Main outcome
- Mechanisms only
Who paid for it
- Funding
- Independent funding
- Government
- National Institute for Health and Care Research
- Government
- National Institutes of Health
- Government
- Korea National Institute of Health
- Grants
- Korea National Institute of Health (4845-302-210-13)
Based on 3 listed funder(s).
Publication
- Published
- 2014-06-18 · FEBS Lett · vol. 588 · issue 17 · pp. 3081–3088
- Publisher
- Wiley
- Cited
- 71 citations · more than 94% of similar papers · 3.5× the field average
- Impact
- Top 10% most cited in its field
- References
- 46 works
- Access
- Free to read
- Research areas
- Genomics, phytochemicals, and oxidative stress · Autophagy in Disease and Therapy · Adenosine and Purinergic Signaling
- Keywords
- Autophagy, Sulforaphane, MAPK/ERK pathway, Activator (genetics), Cell biology, Chemistry, Reactive oxygen species, Gene knockdown, Kinase, Extracellular, Biochemistry, Apoptosis, Biology, Receptor
- MeSH
- neurons, cell line, tumor, animals, humans, mice, reactive oxygen species, isothiocyanates, sulfoxides, extracellular signal-regulated map kinases, enzyme activation, autophagy
8 authors
From KR, US
- Chulman Jo · correspondingKorea National Institute of Health
- Sunhyo KimKorea National Institute of Health
- Sun‐Jung ChoKorea National Institute of Health
- Ki Ju ChoiKorea National Institute of Health
- Sang‐Moon YunKorea National Institute of Health
- Young Ho KohKorea National Institute of Health
Abstract
Sulforaphane (SFN), an activator of nuclear factor E2-related factor 2 (Nrf2), has been reported to induce autophagy in several cells. However, little is known about its signaling mechanism of autophagic induction. Here, we provide evidence that SFN induces autophagy with increased levels of LC3-II through extracellular signal-regulated kinase (ERK) activation in neuronal cells. Pretreatment with NAC (N-acetyl-l-cysteine), a well-known antioxidant, completely blocked the SFN-induced increase in LC3-II levels and activation of ERK. Knockdown or overexpression of Nrf2 did not affect autophagy. Together, the results suggest that SFN-mediated generation of reactive oxygen species (ROS) induces autophagy via ERK activation, independent of Nrf2 activity in neuronal cells.
Abstract via Europe PMC. Copyright remains with the authors or publisher.
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