Sulforaphane induces autophagy through ERK activation in neuronal cells |
| |
Authors: | Chulman Jo Sunhyo Kim Sun-Jung Cho Ki Ju Choi Sang-Moon Yun Young Ho Koh Gail V.W. Johnson Sang Ick Park |
| |
Affiliation: | 1. Division of Brain Diseases, Center for Biomedical Sciences, Korea National Institute of Health, 187 Osongsaengmyeong2(i)-ro, Osong-eup, Cheongwon-gun, Chungcheongbuk-do 363-951, Republic of Korea;2. Division of Respiratory Viruses, Center for Infectious Diseases, Korea National Institute of Health, 187 Osongsaengmyeong2(i)-ro, Osong-eup, Cheongwon-gun, Chungcheongbuk-do 363-951, Republic of Korea;3. Department of Anesthesiology, University of Rochester Medical Center, University of Rochester, 601 Elmwood Ave., Rochester, NY, USA |
| |
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. |
| |
Keywords: | SFN, sulforaphane Nrf2, nuclear factor E2-related factor 2 Keap1, Kelch-like ECH-associated protein 1 ARE, antioxidant response element LC-3, microtubule-associated protein 1 light chain 3 AV, autophagic vesicle ERK, extracellular signal-regulated kinase JNK, c-jun N-terminal kinase SAPK, stress-activated protein kinase MEK, mitogen protein kinase kinase HO-1, heme oxygenase-1 NAC, N-acetyl-l-cysteine DCF-DA, 6-carboxy-2&prime ,7&prime -dichlorodihydrofluorescien diacetate |
本文献已被 ScienceDirect 等数据库收录! |
|