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Sulforaphane induces autophagy through ERK activation in neuronal cells
Author(s) -
Jo Chulman,
Kim Sunhyo,
Cho Sun-Jung,
Choi Ki Ju,
Yun Sang-Moon,
Koh Young Ho,
Johnson Gail V.W.,
Park Sang Ick
Publication year - 2014
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/j.febslet.2014.06.036
Subject(s) - autophagy , sulforaphane , mapk/erk pathway , activator (genetics) , microbiology and biotechnology , chemistry , reactive oxygen species , gene knockdown , kinase , extracellular , apoptosis , biochemistry , biology , receptor
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.