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Role of Galectin-3 in Mast Cell Functions: Galectin-3-Deficient Mast Cells Exhibit Impaired Mediator Release and Defective JNK Expression¹

Huan-Yuan Chen^2,*, Bhavya B. Sharma^2,, Lan Yu^*, Riaz Zuberi^3,, I-Chun Weng^*, Yuko Kawakami, Toshiaki Kawakami, Daniel K. Hsu^* and Fu-Tong Liu^4,*

^* Department of Dermatology, School of Medicine, University of California-Davis, Sacramento, CA 95817; and Division of Cell Biology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121

Galectin-3 is a member of the -galactoside-binding animal lectin family expressed in various cell types, including mast cells. To determine the role of galectin-3 in the function of mast cells, we studied bone marrow-derived mast cells (BMMC) from wild-type (gal3^+/+) and galectin-3-deficient (gal3^–/–) mice. Cells from the two genotypes showed comparable expression of IgE receptor and c-Kit. However, upon activation by FcRI cross-linkage, gal3^–/– BMMC secreted a significantly lower amount of histamine as well as the cytokine IL-4, compared with gal3^+/+ BMMC. In addition, we found significantly reduced passive cutaneous anaphylaxis reactions in gal3^–/– mice compared with gal3^+/+ mice. These results indicate that there is a defect in the response of mast cells in gal3^–/– mice. Unexpectedly, we found that gal3^–/– BMMC contained a dramatically lower basal level of JNK1 protein compared with gal3^+/+ BMMC, which is probably responsible for the lower IL-4 production. The decreased JNK1 level in gal3^–/– BMMC is accompanied by a lower JNK1 mRNA level, suggesting that galectin-3 regulates the transcription of the JNK gene or processing of its RNA. All together, these results point to an important role of galectin-3 in mast cell biology.

The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

¹ This work was supported by National Institutes of Health Grants R01 AI20958, R01 AI39620, and P01 AI50498.

² H.-Y.C. and B.B.S. contributed equally.

³ Current address: La Jolla Institute for Molecular Medicine, 4570 Executive Drive, San Diego CA 92121.

⁴ Address correspondence and reprint requests to Dr. Fu-Tong Liu, Department of Dermatology, School of Medicine, University of California-Davis, 3301 C Street, Suite No. 1400, Sacramento, CA 95816. E-mail address: fliu{at}ucdavis.edu

⁵ Abbreviations used in this paper: CRD, carbohydrate-recognition domain; BMMC, bone marrow-derived mast cell; SCF, stem cell factor; LAT, linker for activation of T cells; PLC, phospholipase C; PKC, protein kinase C; PCA, passive cutaneous anaphylaxis.

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