| Overexpression of Galectin-3 in Macrophages of C57BL/6 mice with Experimental Autoimmune Encephalomyelitis |
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Dae Seung Kim1, Insun Hwang1, Suk-jae Park1, Ginnae Ahn2, Sang-Joon Park3, Hyun Jeong Park1, Hong-Gu Joo1, Youngheun Jee1 |
1College of Veterinary Medicine, Jeju National University
2Faculty of Marine life science, Jeju National University
3College of Veterinary Medicine, Kyungpook National University |
| 자가면역성 뇌척수염을 유도한 C57BL/6 마우스 큰포식세포에서의 Galectin-3의 과발현 |
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김대승1, 황인선1, 박석재1, 안긴내2, 박상준3, 박현정1, 주홍구1, 지영흔1 |
1제주대학교 수의과대학 수의학과
2해양과학대학 해양생명과학과
3경북대학교 수의과대학 수의학과 |
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| Abstract |
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Experimental autoimmune encephalomyelitis (EAE) is an inflammatory disease in the murine central nervous system (CNS) and has long been used as an animal model for human multiple sclerosis. Development of EAE requires coordinated expression of a number of genes that are involved in the activation and effector functions of inflammatory cells. Galectin-3 (Gal-3) is a member of the betagalactoside- binding lectin family and plays an important role in inflammatory responses through its functions on cell activation, cell migration or inhibition of apoptosis. We investigated the functional role of Gal-3 in EAE mice following immunization with myelin oligodendrocyte glycoprotein $(MOG)_{35-55}$ peptide. During the peak stage of EAE, the localization of Gal-3 in inflammatory cells markedly increased in subarachnoid membranes and perivascular regions of CNS. In contrast, Gal-3 was weakly detected in cerebrum and spinal of the recovery stage of EAE. Consistent with this finding, western blot analysis revealed that Gal-3 expression was significantly increased at the peak stage while it was slightly decreased at the recovery stage in the CNS. In addition, the population of $CD11b^{+}$ macrophage expressing Gal- 3 in spleen of EAE mice was markedly increased compared with control mice. In fact, most of activated macrophages isolated from spleen of EAE mice expressed Gal-3. Taken together, our results demonstrate that the over-expression of Gal-3 in activated macrophages may play a key role in promoting inflammatory cells in the CNS during EAE. |
| Key Words:
Central Nervous System, Experimental Autoimmune Encephalomyelitis, Galectin-3, macrophage |
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