[Ca2+]-dependent generation of intracellular reactive oxygen species mediates maitotoxin-induced cellular responses in human umbilical vein endothelial cells

Sun Ju Yi, Kyung Hwan Kim, Hyun Jung Choi, Je Ok Yoo, Hyo il Jung, Jeong A. Han, Young Myeong Kim, In Bum Suh, Kwon Soo Ha

Research output: Contribution to journalArticle

14 Citations (Scopus)

Abstract

Maitotoxin (MTX) is known as one of the most potent marine toxins involved in Ciguatera poisoning, but intracellular signaling pathways caused by MTX was not fully understood. Thus, we have investigated whether intracellular reactive oxygen species (ROS) are involved in MTX-induced cellular responses in human umbilical vein endothelial cells. MTX induced a dose-dependent increase of intracellular [Ca2+]. MTX stimulated the production of intracellular ROS in a dose- and time-dependent manner, which was suppressed by BAPTA-AM, an intracellular Ca2+ chelator. Ionomycin also elevated the ROS production in a dose-dependent manner. MTX elevated transamidation activity in a time-dependent manner and the activation was largely inhibited by transfection of tissue transglutaminase siRNA. The activation of tissue transglutaminase and ERK1/2 by MTX was suppressed by BAPTA-AM or ROS scavengers. In addition, MTX-induced cell death was significantly delayed by BAPTA-AM or a ROS scavenger. These results suggest that [Ca2+]-dependent generation of intracellular ROS, at least in part, play an important role in MTX-stimulated cellular responses, such as activation of tTGase, ERK phosphorylation, and induction of cell death, in human umbilical vein endothelial cells.

Original languageEnglish
Pages (from-to)121-128
Number of pages8
JournalMolecules and Cells
Volume21
Issue number1
Publication statusPublished - 2006 Feb 28

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Human Umbilical Vein Endothelial Cells
Reactive Oxygen Species
Cell Death
Ciguatera Poisoning
Marine Toxins
maitotoxin
Ionomycin
Chelating Agents
Small Interfering RNA
Transfection
Phosphorylation

All Science Journal Classification (ASJC) codes

  • Medicine(all)

Cite this

Yi, Sun Ju ; Kim, Kyung Hwan ; Choi, Hyun Jung ; Yoo, Je Ok ; Jung, Hyo il ; Han, Jeong A. ; Kim, Young Myeong ; Suh, In Bum ; Ha, Kwon Soo. / [Ca2+]-dependent generation of intracellular reactive oxygen species mediates maitotoxin-induced cellular responses in human umbilical vein endothelial cells. In: Molecules and Cells. 2006 ; Vol. 21, No. 1. pp. 121-128.
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abstract = "Maitotoxin (MTX) is known as one of the most potent marine toxins involved in Ciguatera poisoning, but intracellular signaling pathways caused by MTX was not fully understood. Thus, we have investigated whether intracellular reactive oxygen species (ROS) are involved in MTX-induced cellular responses in human umbilical vein endothelial cells. MTX induced a dose-dependent increase of intracellular [Ca2+]. MTX stimulated the production of intracellular ROS in a dose- and time-dependent manner, which was suppressed by BAPTA-AM, an intracellular Ca2+ chelator. Ionomycin also elevated the ROS production in a dose-dependent manner. MTX elevated transamidation activity in a time-dependent manner and the activation was largely inhibited by transfection of tissue transglutaminase siRNA. The activation of tissue transglutaminase and ERK1/2 by MTX was suppressed by BAPTA-AM or ROS scavengers. In addition, MTX-induced cell death was significantly delayed by BAPTA-AM or a ROS scavenger. These results suggest that [Ca2+]-dependent generation of intracellular ROS, at least in part, play an important role in MTX-stimulated cellular responses, such as activation of tTGase, ERK phosphorylation, and induction of cell death, in human umbilical vein endothelial cells.",
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[Ca2+]-dependent generation of intracellular reactive oxygen species mediates maitotoxin-induced cellular responses in human umbilical vein endothelial cells. / Yi, Sun Ju; Kim, Kyung Hwan; Choi, Hyun Jung; Yoo, Je Ok; Jung, Hyo il; Han, Jeong A.; Kim, Young Myeong; Suh, In Bum; Ha, Kwon Soo.

In: Molecules and Cells, Vol. 21, No. 1, 28.02.2006, p. 121-128.

Research output: Contribution to journalArticle

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