Amurensin G induces autophagy and attenuates cellular toxicities in a rotenone model of Parkinson's disease

Hyun Wook Ryu, Won Keun Oh, Ik Soon Jang, Junsoo Park

Research output: Contribution to journalArticle

19 Citations (Scopus)

Abstract

Although Parkinson's disease is a common neurodegenerative disorder its cause is still unknown. Recently, several reports showed that inducers of autophagy attenuate cellular toxicities in Parkinson's disease models. In this report we screened HEK293 cells that stably express GFP-LC3, a marker of autophagy, for autophagy inducers and identified amurensin G, a compound isolated from the wild grape (. Vitis amurensis). Amurensin G treatment induced punctate cytoplasmic expression of GFP-LC3 and increased the expression level of endogenous LC3-II. Incubation of human dopaminergic SH-SY5Y cells with amurensin G attenuated the cellular toxicities of rotenone in a model of Parkinson's disease. Amurensin G inhibited rotenone-induced apoptosis and interfered with rotenone-induced G2/M cell cycle arrest. In addition, knockdown of beclin1, a regulator of autophagy, abolished the effect of amurensin G. These data collectively indicate that amurensin G attenuates cellular toxicities through the induction of autophagy.

Original languageEnglish
Pages (from-to)121-126
Number of pages6
JournalBiochemical and Biophysical Research Communications
Volume433
Issue number1
DOIs
Publication statusPublished - 2013 Mar 29

Fingerprint

Rotenone
Autophagy
Parkinson Disease
Toxicity
Vitis
G2 Phase Cell Cycle Checkpoints
HEK293 Cells
Neurodegenerative Diseases
amurensin G
Cells
Apoptosis

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology

Cite this

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Amurensin G induces autophagy and attenuates cellular toxicities in a rotenone model of Parkinson's disease. / Ryu, Hyun Wook; Oh, Won Keun; Jang, Ik Soon; Park, Junsoo.

In: Biochemical and Biophysical Research Communications, Vol. 433, No. 1, 29.03.2013, p. 121-126.

Research output: Contribution to journalArticle

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