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Overexpression of Galectin-3 in Macrophages of C57BL/6 mice with Experimental Autoimmune Encephalomyelitis

자가면역성 뇌척수염을 유도한 C57BL/6 마우스 큰포식세포에서의 Galectin-3의 과발현

  • Kim, Dae Seung (College of Veterinary Medicine, Jeju National University) ;
  • Hwang, Insun (College of Veterinary Medicine, Jeju National University) ;
  • Park, Suk-jae (College of Veterinary Medicine, Jeju National University) ;
  • Ahn, Ginnae (Faculty of Marine life science, Jeju National University) ;
  • Park, Sang-Joon (College of Veterinary Medicine, Kyungpook National University) ;
  • Park, Hyun Jeong (College of Veterinary Medicine, Jeju National University) ;
  • Joo, Hong-Gu (College of Veterinary Medicine, Jeju National University) ;
  • Jee, Youngheun (College of Veterinary Medicine, Jeju National University)
  • 김대승 (제주대학교 수의과대학 수의학과) ;
  • 황인선 (제주대학교 수의과대학 수의학과) ;
  • 박석재 (제주대학교 수의과대학 수의학과) ;
  • 안긴내 (해양과학대학 해양생명과학과) ;
  • 박상준 (경북대학교 수의과대학 수의학과) ;
  • 박현정 (제주대학교 수의과대학 수의학과) ;
  • 주홍구 (제주대학교 수의과대학 수의학과) ;
  • 지영흔 (제주대학교 수의과대학 수의학과)
  • Accepted : 2011.03.14
  • Published : 2011.06.30

Abstract

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.

Keywords

Acknowledgement

Supported by : 한국연구재단

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