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Title: Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption

Abstract

Lipid rafts are plasma membrane platforms mediating signal transduction pathways for cellular proliferation, differentiation and apoptosis. Here, we show that membrane fluidity was increased in HeLa cells following treatment with ginsenoside Rh2 (Rh2), as determined by cell staining with carboxy-laurdan (C-laurdan), a two-photon dye designed for measuring membrane hydrophobicity. In the presence of Rh2, caveolin-1 appeared in non-raft fractions after sucrose gradient ultracentrifugation. In addition, caveolin-1 and GM1, lipid raft landmarkers, were internalized within cells after exposure to Rh2, indicating that Rh2 might disrupt lipid rafts. Since cholesterol overloading, which fortifies lipid rafts, prevented an increase in Rh2-induced membrane fluidity, caveolin-1 internalization and apoptosis, lipid rafts appear to be essential for Rh2-induced apoptosis. Moreover, Rh2-induced Fas oligomerization was abolished following cholesterol overloading, and Rh2-induced apoptosis was inhibited following treatment with siRNA for Fas. This result suggests that Rh2 is a novel lipid raft disruptor leading to Fas oligomerization and apoptosis.

Authors:
;  [1];  [2];  [3];  [4];  [1];  [1]
  1. College of Life Sciences and Biotechnology, Korea University, 1, 5-ka, Anam-dong, Sungbuk-gu, Seoul 136-701 (Korea, Republic of)
  2. Department of Chemistry, Korea University, Seoul 136-701 (Korea, Republic of)
  3. Department of Chemistry, Ajou University, Suwon, Kyunggi-Do 443-749 (Korea, Republic of)
  4. Division of Specific Organs Center, National Cancer Center, Kyunggi-Do 411-769 (Korea, Republic of)
Publication Date:
OSTI Identifier:
22199742
Resource Type:
Journal Article
Journal Name:
Biochemical and Biophysical Research Communications
Additional Journal Information:
Journal Volume: 385; Journal Issue: 2; Other Information: Copyright (c) 2009 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved.; Country of input: International Atomic Energy Agency (IAEA); Journal ID: ISSN 0006-291X
Country of Publication:
United States
Language:
English
Subject:
60 APPLIED LIFE SCIENCES; APOPTOSIS; CELL PROLIFERATION; CHOLESTEROL; HELA CELLS; LIGANDS; LIPIDS; PHOTONS; SACCHAROSE; ULTRACENTRIFUGATION

Citation Formats

Yi, Jae-Sung, Choo, Hyo-Jung, Cho, Bong-Rae, Kim, Hwan-Myung, Kim, Yong-Nyun, Ham, Young-Mi, and Ko, Young-Gyu. Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption. United States: N. p., 2009. Web. doi:10.1016/J.BBRC.2009.05.028.
Yi, Jae-Sung, Choo, Hyo-Jung, Cho, Bong-Rae, Kim, Hwan-Myung, Kim, Yong-Nyun, Ham, Young-Mi, & Ko, Young-Gyu. Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption. United States. doi:10.1016/J.BBRC.2009.05.028.
Yi, Jae-Sung, Choo, Hyo-Jung, Cho, Bong-Rae, Kim, Hwan-Myung, Kim, Yong-Nyun, Ham, Young-Mi, and Ko, Young-Gyu. Fri . "Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption". United States. doi:10.1016/J.BBRC.2009.05.028.
@article{osti_22199742,
title = {Ginsenoside Rh2 induces ligand-independent Fas activation via lipid raft disruption},
author = {Yi, Jae-Sung and Choo, Hyo-Jung and Cho, Bong-Rae and Kim, Hwan-Myung and Kim, Yong-Nyun and Ham, Young-Mi and Ko, Young-Gyu},
abstractNote = {Lipid rafts are plasma membrane platforms mediating signal transduction pathways for cellular proliferation, differentiation and apoptosis. Here, we show that membrane fluidity was increased in HeLa cells following treatment with ginsenoside Rh2 (Rh2), as determined by cell staining with carboxy-laurdan (C-laurdan), a two-photon dye designed for measuring membrane hydrophobicity. In the presence of Rh2, caveolin-1 appeared in non-raft fractions after sucrose gradient ultracentrifugation. In addition, caveolin-1 and GM1, lipid raft landmarkers, were internalized within cells after exposure to Rh2, indicating that Rh2 might disrupt lipid rafts. Since cholesterol overloading, which fortifies lipid rafts, prevented an increase in Rh2-induced membrane fluidity, caveolin-1 internalization and apoptosis, lipid rafts appear to be essential for Rh2-induced apoptosis. Moreover, Rh2-induced Fas oligomerization was abolished following cholesterol overloading, and Rh2-induced apoptosis was inhibited following treatment with siRNA for Fas. This result suggests that Rh2 is a novel lipid raft disruptor leading to Fas oligomerization and apoptosis.},
doi = {10.1016/J.BBRC.2009.05.028},
journal = {Biochemical and Biophysical Research Communications},
issn = {0006-291X},
number = 2,
volume = 385,
place = {United States},
year = {2009},
month = {7}
}