CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells.

CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells. Research Abstract Details 

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CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells. Abstract Text:

Tomohiro Yamanishi,Yoshiko Yamamoto,Tomomitsu Hatakeyama,Kenichi Yamaguchi,Tatsuya Oda,Tomohiro Yamanishi,Yoshiko Yamamoto,Tomomitsu Hatakeyama,Kenichi Yamaguchi,Tatsuya Oda,Tomohiro Yamanishi,Yoshiko Yamamoto,Tomomitsu Hatakeyama,Kenichi Yamaguchi,Tatsuya Oda,

Our previous studies demonstrated that CEL-I, an N-acetylgalactosamine (GalNAc)-specific C-type lectin purified from the marine invertebrate Cucumaria echinata (Holothuroidea) showed potent cytotoxicity to several cell lines such as HeLa, MDCK and XC cells. In this study, we found that CEL-I induced increased secretion of tumour necrosis factor-alpha (TNF-alpha) and granulocyte colony stimulation factor (G-CSF) by mouse macrophage cell line RAW264.7 cells in a dose-dependent manner, whereas this cell line was highly resistant to CEL-I cytotoxicity. The cytokine-inducing activity of CEL-I was stronger than that of phytohaemagglutinin (PHA-L). A binding study using FITC-labelled CEL-I (F-CEL-I) indicated that the amount of bound F-CEL-I on RAW264.7 cells was greater than that of F-PHA-L, suggesting that the greater activity of CEL-I to induce cytokine secretion by RAW264.7 cells is partly due to the higher binding ability. Since the cell binding and cytokine-inducing activity of CEL-I were partly but significantly inhibited by the specific sugar (GalNAc), it is considered that the binding of CEL-I to cell-surface-specific saccharide moieties, which may be recognized by CEL-I with higher affinity than GalNAc, is essential for the induction of cytokine secretion. The secretion of TNF-alpha and G-CSF from CEL-I-treated RAW264.7 cells were almost completely prevented by brefeldin A (BFA), whereas increase in mRNA levels of these cytokines were not affected by BFA. Bio-Plex beads assay suggested that temporal increase in phosphorylation of extracellular-regulated kinase (ERK), c-jun NH(2)-terminal kinase (JNK) and p38 MAP kinase occurred at relatively early time following CEL-I treatment. Furthermore, the secretion of TNF-alpha and G-CSF were inhibited by specific inhibitors for these MAP kinases. These results suggest that the intracellular signal transduction through the activation of MAP kinase system is involved in CEL-I-induced cytokine secretion.

CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells. Publishing Authors By Initials

T Yamanishi,Y Yamamoto,T Hatakeyama,K Yamaguchi,T Oda,T Yamanishi,Y Yamamoto,T Hatakeyama,K Yamaguchi,T Oda,T Yamanishi,Y Yamamoto,T Hatakeyama,K Yamaguchi,T Oda,

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CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells. Journal Published:

PUBLICATION TYPE: Journal Article

Journal: Journal of biochemistry

VOLUME: 142

Page Numbers: 587-95

Journal Abbreviation: J. Biochem.

ISSN: 0021-924X

DAY: 10

MONTH: 09

YEAR: 2007

CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells. Information

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LANGUAGE: eng

NlmUniqueID: 376600

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Grant and Affiliation Information for CEL-I, an Invertebrate N-Acetylgalactosamine-specific C-Type Lectin, Induces TNF-{alpha} and G-CSF Production by Mouse Macrophage Cell Line RAW264.7 Cells.

AFFILIATION: Division of Biochemistry, Faculty of Fisheries and Department of Applied Chemistry, Faculty of Engineering, Nagasaki University, 1-14 Bunkyo-machi, Nagasaki 852-8521, Japan.

Country: Japan

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MEDLINETA: J Biochem (Tokyo)

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