Eotaxin induces migration of RBL-2H3 mast cells via a Rac-ERK-dependent pathway

Chang Hoon Woo; Dong Tak Jeong; Seog Beom Yoon; Key Sun Kim; Il Yup Chung; Toshihiko Saeki; Jae Hong Kim

doi:10.1016/S0006-291X(02)02432-4

Eotaxin induces migration of RBL-2H3 mast cells via a Rac-ERK-dependent pathway

Chang Hoon Woo, Dong Tak Jeong, Seog Beom Yoon, Key Sun Kim, Il Yup Chung, Toshihiko Saeki, Jae Hong Kim

Division of life Sciences

Research output: Contribution to journal › Article › peer-review

36 Citations (Scopus)

Abstract

Eotaxin is a potent chemokine that acts via CC chemokine receptor 3 (CCR3)to induce chemotaxis, mainly on eosinophils. Here we show that eotaxin also induces chemotactic migration in rat basophilic leukemia (RBL-2H3) mast cells. This effect was dose-dependently inhibited by compound X, a selective CCR3 antagonist, indicating that, as in eosinophils, the effect was mediated by CCR3. Eotaxin-induced cell migration was completely blocked in RBL-RacN17 cells expressing adominant negative Rac1 mutant, suggesting a crucial role for Rac1 in eotaxin signaling to chemotactic migration. ERK activation also proved essential for eotaxin signaling and it too was absent in RBL-RacN17 cells. Finally, we found that activation of Rac and ERK was correlated with eotaxin-induced actin reorganization known to be necessary for cell motility. It thus appears that Rac1 acts upstream of ERK to signal chemotaxis in these cells, and that a Rac-ERK-dependent cascade mediates the eotaxin-induced chemotactic motility of RBL-2H3 mast cells.

Original language	English
Pages (from-to)	392-397
Number of pages	6
Journal	Biochemical and biophysical research communications
Volume	298
Issue number	3
DOIs	https://doi.org/10.1016/S0006-291X(02)02432-4
Publication status	Published - 2002

Bibliographical note

Funding Information:
This work was supported by a Korea University Grant (2002, to J.H. Kim) and grants from the Basic Research Program (RO2-2002-000-00029-0), the Interdisciplinary Research Program (R01-1999-00097), the SRC program (Aging and Apoptosis Research Center) to Seoul National University, College of Medicine (2002) of the Korea Science and Engineering Foundation (KOSEF), and the Proteomics (Frontier 21) Project from the Ministry of Science and Technology.

Keywords

Chemotaxis
ERK
Eotaxin
RBL-2H3
Rac

ASJC Scopus subject areas

Biophysics
Biochemistry
Molecular Biology
Cell Biology

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10.1016/S0006-291X(02)02432-4

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title = "Eotaxin induces migration of RBL-2H3 mast cells via a Rac-ERK-dependent pathway",

abstract = "Eotaxin is a potent chemokine that acts via CC chemokine receptor 3 (CCR3)to induce chemotaxis, mainly on eosinophils. Here we show that eotaxin also induces chemotactic migration in rat basophilic leukemia (RBL-2H3) mast cells. This effect was dose-dependently inhibited by compound X, a selective CCR3 antagonist, indicating that, as in eosinophils, the effect was mediated by CCR3. Eotaxin-induced cell migration was completely blocked in RBL-RacN17 cells expressing adominant negative Rac1 mutant, suggesting a crucial role for Rac1 in eotaxin signaling to chemotactic migration. ERK activation also proved essential for eotaxin signaling and it too was absent in RBL-RacN17 cells. Finally, we found that activation of Rac and ERK was correlated with eotaxin-induced actin reorganization known to be necessary for cell motility. It thus appears that Rac1 acts upstream of ERK to signal chemotaxis in these cells, and that a Rac-ERK-dependent cascade mediates the eotaxin-induced chemotactic motility of RBL-2H3 mast cells.",

keywords = "Chemotaxis, ERK, Eotaxin, RBL-2H3, Rac",

author = "Woo, {Chang Hoon} and {Tak Jeong}, Dong and Yoon, {Seog Beom} and Kim, {Key Sun} and {Yup Chung}, Il and Toshihiko Saeki and Kim, {Jae Hong}",

note = "Funding Information: This work was supported by a Korea University Grant (2002, to J.H. Kim) and grants from the Basic Research Program (RO2-2002-000-00029-0), the Interdisciplinary Research Program (R01-1999-00097), the SRC program (Aging and Apoptosis Research Center) to Seoul National University, College of Medicine (2002) of the Korea Science and Engineering Foundation (KOSEF), and the Proteomics (Frontier 21) Project from the Ministry of Science and Technology.",

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doi = "10.1016/S0006-291X(02)02432-4",

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AU - Woo, Chang Hoon

AU - Tak Jeong, Dong

AU - Yoon, Seog Beom

AU - Kim, Key Sun

AU - Yup Chung, Il

AU - Saeki, Toshihiko

AU - Kim, Jae Hong

N1 - Funding Information: This work was supported by a Korea University Grant (2002, to J.H. Kim) and grants from the Basic Research Program (RO2-2002-000-00029-0), the Interdisciplinary Research Program (R01-1999-00097), the SRC program (Aging and Apoptosis Research Center) to Seoul National University, College of Medicine (2002) of the Korea Science and Engineering Foundation (KOSEF), and the Proteomics (Frontier 21) Project from the Ministry of Science and Technology.

PY - 2002

Y1 - 2002

N2 - Eotaxin is a potent chemokine that acts via CC chemokine receptor 3 (CCR3)to induce chemotaxis, mainly on eosinophils. Here we show that eotaxin also induces chemotactic migration in rat basophilic leukemia (RBL-2H3) mast cells. This effect was dose-dependently inhibited by compound X, a selective CCR3 antagonist, indicating that, as in eosinophils, the effect was mediated by CCR3. Eotaxin-induced cell migration was completely blocked in RBL-RacN17 cells expressing adominant negative Rac1 mutant, suggesting a crucial role for Rac1 in eotaxin signaling to chemotactic migration. ERK activation also proved essential for eotaxin signaling and it too was absent in RBL-RacN17 cells. Finally, we found that activation of Rac and ERK was correlated with eotaxin-induced actin reorganization known to be necessary for cell motility. It thus appears that Rac1 acts upstream of ERK to signal chemotaxis in these cells, and that a Rac-ERK-dependent cascade mediates the eotaxin-induced chemotactic motility of RBL-2H3 mast cells.

AB - Eotaxin is a potent chemokine that acts via CC chemokine receptor 3 (CCR3)to induce chemotaxis, mainly on eosinophils. Here we show that eotaxin also induces chemotactic migration in rat basophilic leukemia (RBL-2H3) mast cells. This effect was dose-dependently inhibited by compound X, a selective CCR3 antagonist, indicating that, as in eosinophils, the effect was mediated by CCR3. Eotaxin-induced cell migration was completely blocked in RBL-RacN17 cells expressing adominant negative Rac1 mutant, suggesting a crucial role for Rac1 in eotaxin signaling to chemotactic migration. ERK activation also proved essential for eotaxin signaling and it too was absent in RBL-RacN17 cells. Finally, we found that activation of Rac and ERK was correlated with eotaxin-induced actin reorganization known to be necessary for cell motility. It thus appears that Rac1 acts upstream of ERK to signal chemotaxis in these cells, and that a Rac-ERK-dependent cascade mediates the eotaxin-induced chemotactic motility of RBL-2H3 mast cells.

KW - Chemotaxis

KW - ERK

KW - Eotaxin

KW - RBL-2H3

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IS - 3

ER -

Eotaxin induces migration of RBL-2H3 mast cells via a Rac-ERK-dependent pathway

Abstract

Bibliographical note

Keywords

ASJC Scopus subject areas

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