Physiology: Indole-3-carbinol prevents H2O2-induced inhibition of gap junctional intercellular communication by inactivation of PKB/Akt

• HWANG Jae-Woong

  Laboratory of Stem Cell and Tumor Biology, Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University

• JUNG Ji-Won

  Laboratory of Stem Cell and Tumor Biology, Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University

• LEE Yong-Soon

  Laboratory of Stem Cell and Tumor Biology, Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University

• KANG Kyung-Sun

  Laboratory of Stem Cell and Tumor Biology, Department of Veterinary Public Health, College of Veterinary Medicine, Seoul National University

書誌事項

タイトル別名

• Indole-3-Carbinol Prevents H2O2-Induced Inhibition of Gap Junctional Intercellular Communication by Inactivation of PKB/Akt

抄録

Indole-3-carbinol (I3C) is a phytochemical found in cruciferous vegetables and possesses a variety of biological and biochemical effects. Despite a wealth of data about the chemopreventive properties of I3C, its effects on gap junctional intercellular communication (GJIC), which is associated with the promotion and progression phases of the multi-stage process of carcinogenesis, has not been studied. In this study, we examined the ability of I3C to prevent H₂O ₂-induced inhibition of GJIC in WB-F344 rat liver epithelial cells (WB cells). The cells were preincubated with I3C for 48 hr, and then treated with 1 mM H₂O₂ for 1 hr. We found that I3C could prevent the H₂O₂-induced inhibition of GJIC through prevention of the phosphorylated state of gap junction protein connexin 43 (Cx43) phosphorylation. Prevention of GJIC by I3C was dependent upon inactivation of Akt, but not MAPK, although inhibition of GJIC by H₂O₂ leads to activation of both. Similar to I3C, modulation of Akt activation through the phosphoinositide-3 kinase inhibitor, LY294002, could also prevent H₂O₂-induced inhibition of GJIC and phosphorylation of Cx43. Our results suggest that I3C might exert its dietary chemopreventive effects by interfering with the Akt signaling pathway, which appears to be linked to modulating GJIC, a cellular mechanisms regulating cell proliferation, differentiation and apoptosis.<br>

収録刊行物

• Ｔｈｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｖｅｔｅｒｉｎａｒｙ　Ｍｅｄｉｃａｌ　Ｓｃｉｅｎｃｅ

  Ｔｈｅ　Ｊｏｕｒｎａｌ　ｏｆ　Ｖｅｔｅｒｉｎａｒｙ　Ｍｅｄｉｃａｌ　Ｓｃｉｅｎｃｅ 70 (10), 1057-1063, 2008

  公益社団法人 日本獣医学会

キーワード

• gap junctional intercellular communication
• indole-3-carbinol
• oxidative stress
• PKB/Akt

詳細情報

• CRID: 1390282681406345216
• NII論文ID: 110006967088
• NII書誌ID: AA10796138
• DOI: 10.1292/jvms.70.1057
• ISSN: 13477439
• ISSN: 09167250
• NDL書誌ID: 9691287
• Web Site: https://ndlsearch.ndl.go.jp/books/R000000004-I9691287
• Web Site: http://www.jstage.jst.go.jp/article/jvms/70/10/70_10_1057/_pdf
• Web Site: https://search.jamas.or.jp/link/ui/2009021437
• 本文言語コード: en
• データソース種別:
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