Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells

Jesang Ko; In Sik Kim; Sung Wuk Jang; Young Han Lee; Soon Young Shin; Do Sik Min; Doe Sun Na

doi:10.1016/S0014-5793(02)02465-1

Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells

Jesang Ko, In Sik Kim, Sung Wuk Jang, Young Han Lee, Soon Young Shin, Do Sik Min, Doe Sun Na

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

13 Citations (Scopus)

Abstract

Leukotactin-1 (Lkn-1)/CCL15 is a recently cloned CC-chemokine that binds to the CCR1 and CCR3. Although Lkn-1 has been known to function as a chemoattractant for neutrophils, monocytes and lymphocytes, its cellular mechanism remains unclear. To understand the mechanism of Lkn-1-induced chemotaxis signaling, we examined the chemotactic activities of human osteogenic sarcoma cells expressing CCR1 in response to Lkn-1 using inhibitors of signaling molecules. Inhibitors of G_i/G_o protein, phospholipase C (PLC) and protein kinase Cδ (PKCδ) inhibited the chemotactic activity of Lkn-1 indicating that Lkn-1-induced chemotaxis signal is transduced through G_i/G_o protein, PLC and PKCδ. The activities of PLC and PKCδ were also enhanced by Lkn-1 stimulation. Chemotactic activity of Lkn-1 was inhibited by the treatment of cycloheximide and actinomycin D suggesting that newly synthesized proteins are needed for chemotaxis. Nuclear factor-κB (NF-κB) inhibitor reduced chemotactic activity of Lkn-1. DNA binding activity of NF-κB was also enhanced by Lkn-1 stimulation. These results suggest that Lkn-1 transduces the signal through G_i/G_o protein, PLC, PKCδ, NF-κB and newly synthesized proteins for chemotaxis.

Original language	English
Pages (from-to)	159-164
Number of pages	6
Journal	FEBS Letters
Volume	515
Issue number	1-3
DOIs	https://doi.org/10.1016/S0014-5793(02)02465-1
Publication status	Published - 2002 Mar 27
Externally published	Yes

Keywords

Chemokine
Nuclear factor-κB
Phospholipase C
Protein kinase C

ASJC Scopus subject areas

Biophysics
Structural Biology
Biochemistry
Molecular Biology
Genetics
Cell Biology

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10.1016/S0014-5793(02)02465-1

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@article{b943d9ab902e4e1081a816a627067b12,

title = "Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells",

abstract = "Leukotactin-1 (Lkn-1)/CCL15 is a recently cloned CC-chemokine that binds to the CCR1 and CCR3. Although Lkn-1 has been known to function as a chemoattractant for neutrophils, monocytes and lymphocytes, its cellular mechanism remains unclear. To understand the mechanism of Lkn-1-induced chemotaxis signaling, we examined the chemotactic activities of human osteogenic sarcoma cells expressing CCR1 in response to Lkn-1 using inhibitors of signaling molecules. Inhibitors of Gi/Go protein, phospholipase C (PLC) and protein kinase Cδ (PKCδ) inhibited the chemotactic activity of Lkn-1 indicating that Lkn-1-induced chemotaxis signal is transduced through Gi/Go protein, PLC and PKCδ. The activities of PLC and PKCδ were also enhanced by Lkn-1 stimulation. Chemotactic activity of Lkn-1 was inhibited by the treatment of cycloheximide and actinomycin D suggesting that newly synthesized proteins are needed for chemotaxis. Nuclear factor-κB (NF-κB) inhibitor reduced chemotactic activity of Lkn-1. DNA binding activity of NF-κB was also enhanced by Lkn-1 stimulation. These results suggest that Lkn-1 transduces the signal through Gi/Go protein, PLC, PKCδ, NF-κB and newly synthesized proteins for chemotaxis.",

keywords = "Chemokine, Nuclear factor-κB, Phospholipase C, Protein kinase C",

author = "Jesang Ko and Kim, {In Sik} and Jang, {Sung Wuk} and Lee, {Young Han} and Shin, {Soon Young} and Min, {Do Sik} and Na, {Doe Sun}",

note = "Funding Information: This work was supported by the research fund to Immunomodulation Research Center, University of Ulsan from Korea Science and Engineering Foundation (KOSEF).",

year = "2002",

month = mar,

day = "27",

doi = "10.1016/S0014-5793(02)02465-1",

language = "English",

volume = "515",

pages = "159--164",

journal = "FEBS Letters",

issn = "0014-5793",

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number = "1-3",

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TY - JOUR

T1 - Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells

AU - Ko, Jesang

AU - Kim, In Sik

AU - Jang, Sung Wuk

AU - Lee, Young Han

AU - Shin, Soon Young

AU - Min, Do Sik

AU - Na, Doe Sun

N1 - Funding Information: This work was supported by the research fund to Immunomodulation Research Center, University of Ulsan from Korea Science and Engineering Foundation (KOSEF).

PY - 2002/3/27

Y1 - 2002/3/27

N2 - Leukotactin-1 (Lkn-1)/CCL15 is a recently cloned CC-chemokine that binds to the CCR1 and CCR3. Although Lkn-1 has been known to function as a chemoattractant for neutrophils, monocytes and lymphocytes, its cellular mechanism remains unclear. To understand the mechanism of Lkn-1-induced chemotaxis signaling, we examined the chemotactic activities of human osteogenic sarcoma cells expressing CCR1 in response to Lkn-1 using inhibitors of signaling molecules. Inhibitors of Gi/Go protein, phospholipase C (PLC) and protein kinase Cδ (PKCδ) inhibited the chemotactic activity of Lkn-1 indicating that Lkn-1-induced chemotaxis signal is transduced through Gi/Go protein, PLC and PKCδ. The activities of PLC and PKCδ were also enhanced by Lkn-1 stimulation. Chemotactic activity of Lkn-1 was inhibited by the treatment of cycloheximide and actinomycin D suggesting that newly synthesized proteins are needed for chemotaxis. Nuclear factor-κB (NF-κB) inhibitor reduced chemotactic activity of Lkn-1. DNA binding activity of NF-κB was also enhanced by Lkn-1 stimulation. These results suggest that Lkn-1 transduces the signal through Gi/Go protein, PLC, PKCδ, NF-κB and newly synthesized proteins for chemotaxis.

AB - Leukotactin-1 (Lkn-1)/CCL15 is a recently cloned CC-chemokine that binds to the CCR1 and CCR3. Although Lkn-1 has been known to function as a chemoattractant for neutrophils, monocytes and lymphocytes, its cellular mechanism remains unclear. To understand the mechanism of Lkn-1-induced chemotaxis signaling, we examined the chemotactic activities of human osteogenic sarcoma cells expressing CCR1 in response to Lkn-1 using inhibitors of signaling molecules. Inhibitors of Gi/Go protein, phospholipase C (PLC) and protein kinase Cδ (PKCδ) inhibited the chemotactic activity of Lkn-1 indicating that Lkn-1-induced chemotaxis signal is transduced through Gi/Go protein, PLC and PKCδ. The activities of PLC and PKCδ were also enhanced by Lkn-1 stimulation. Chemotactic activity of Lkn-1 was inhibited by the treatment of cycloheximide and actinomycin D suggesting that newly synthesized proteins are needed for chemotaxis. Nuclear factor-κB (NF-κB) inhibitor reduced chemotactic activity of Lkn-1. DNA binding activity of NF-κB was also enhanced by Lkn-1 stimulation. These results suggest that Lkn-1 transduces the signal through Gi/Go protein, PLC, PKCδ, NF-κB and newly synthesized proteins for chemotaxis.

KW - Chemokine

KW - Nuclear factor-κB

KW - Phospholipase C

KW - Protein kinase C

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U2 - 10.1016/S0014-5793(02)02465-1

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AN - SCOPUS:0037181475

SN - 0014-5793

VL - 515

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EP - 164

JO - FEBS Letters

JF - FEBS Letters

IS - 1-3

ER -

Leukotactin-1/CCL15-induced chemotaxis signaling through CCR1 in HOS cells

Abstract

Keywords

ASJC Scopus subject areas

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