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| Content Provider | World Health Organization (WHO)-Global Index Medicus |
|---|---|
| Author | Welsh, C. Jane Smith, Roger Steelman, Andrew J. Li, Jianrong |
| Description | Author Affiliation: Steelman AJ ( Department of Veterinary Integrative Biosciences, College of Veterinary Medicine and Biomedical Sciences, Texas A&M University, College Station, Texas 77843, USA.) |
| Abstract | Demyelination and axonal damage in multiple sclerosis (MS) are thought to be a consequence of inflammatory processes that are perpetuated by activated glia and infiltrating leukocytes. Galectin-9 is a ß-galactoside binding lectin capable of modulating immune responses and appears to be up-regulated in MS. However, its role in the pathogenesis of MS has yet to be determined. Here, we report that proinflammatory cytokines induce galectin-9 (Gal-9) expression in primary astrocytes and the mechanism by which TNF up-regulates Gal-9. Astrocytes did not express Gal-9 under basal conditions nor did IL-6, IL-10, or IL-13 trigger Gal-9 expression. In contrast, IL-1ß, IFN-γ, and particularly TNF up-regulated Gal-9 in astrocytes. TNF-induced Gal-9 expression was dependent on TNF receptor 1 (TNFR1) as TNF failed to induce Gal-9 in TNFR1(-/-) astrocytes. Blockade of the JNK MAP kinase pathway with the JNK inhibitor SP600125 abrogated TNF-induced Gal-9, whereas p38 and MEK inhibitors had minimal effects. Furthermore, specific knockdown of c-Jun via siRNA in astrocytes before TNF treatment greatly suppressed Gal-9 transcription, suggesting that TNF induces astroglial Gal-9 through the TNF/TNFR1/JNK/cJun signaling pathway. Finally, utilizing astrocytes from Lgals9 mutant (Gal-9(-/-)) mice as well as a myelin basic protein-specific Tim-3(+) encephalitogenic T-cell clone (LCN-8), we found that conditioned medium from TNF-stimulated Gal-9(+/+) but not Gal-9(-/-) astrocytes increased the percentage of apoptotic encephalitogenic T-cells. Together, our results suggest that Gal-9 is induced in astrocytes by TNF via the JNK/c-Jun pathway and that astrocyte-derived Gal-9 may function as an immunoregulatory protein in response to ongoing neuroinflammation. |
| ISSN | 00219258 |
| e-ISSN | 1083351X |
| Journal | Journal of Biological Chemistry |
| Issue Number | 33 |
| Volume Number | 288 |
| Language | English |
| Publisher | American Society for Biochemistry and Molecular Biology (United States) |
| Publisher Date | 2013-08-16 |
| Publisher Place | United States |
| Access Restriction | Open |
| Subject Keyword | Apoptosis Drug Effects Astrocytes Metabolism Encephalitis Pathology Galectins T-Lymphocytes Tumor Necrosis Factor-alpha Pharmacology Up-Regulation Animals Genetics Cells, Cultured Enzyme Activation Deficiency Inflammation Mediators JNK Mitogen-Activated Protein Kinases MAP Kinase Signaling System Mice Rats, Sprague-Dawley Receptors, Tumor Necrosis Factor Sus Scrofa Transcription, Genetic Research Support, N.I.H., Extramural Research Support, Non-U.S. Gov't Biochemistry Molecular Biology |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Biochemistry Molecular Biology |
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