| Autor: |
Chabot, Sophie, Kashio, Yumiko, Seki, Masako, Shirato, Yukako, Nakamura, Kazuhiro, Nishi, Nozomu, Nakamura, Takanori, Matsumoto, Ryoji, Hirashima, Mitsuomi |
| Zdroj: |
Glycobiology; Feb2002, Vol. 12 Issue 2, p111-118, 8p |
| Abstrakt: |
Ecalectin/galectin-9 was recently describedas a novel eosinophil chemoattractant highly expressed in immune tissues.We investigated the regulation of galectin-9 expression and releasein Jurkat (a T cell line) cells. We demonstrated that medium andlong-sized galectin-9 isoforms were constitutively expressed, andphorbol 12-myriastate 13-acetate (PMA) upregulated the level ofgalectin-9 mRNA in Jurkat cells. Western blotting and flow cytometryanalyses revealed that PMA stimulation resulted in the upregulationof both intracellular and surface galectin-9 protein. The stimulated Jurkatcells simultaneously released evident eosinophil chemoattractantactivity (ECA). Main ECA was adsorbed by both lactose and anti-galectin-9antibody affinity column, suggesting that the ECA was ascribed togalectin-9. When Jurkat cells were stimulated with PMA in the presenceof a BB94, a matrix metalloproteinase (MMP) inhibitor, but not tissueinhibitor of metalloproteinase-1 (TIMP-1), the release of galectin-9was suppressed in a dose-dependent manner. We further found thatcalphostin c, a protein kinase c (PKC) inhibitor, weakly but significantly suppressedthe release of galectin-9. The present data suggested that galectin-9production in Jurkat cells is provoked by the stimulation with PMAand that some MMP and PKC is, at least, partly involved in the releaseof galectin-9 from Jurkat cells. [ABSTRACT FROM PUBLISHER] |
| Databáze: |
Complementary Index |
| Externí odkaz: |
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