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Expression of galectin-3 in the spinal cords of Lewis rats andNOD mice with experimental autoimmune encephalomyelitis  

Kim, Heechul (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Joo, Hong-Gu (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Moon, Changjong (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Ahn, Meejung (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Jee, Youngheun (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Lim, Yoon-kyu (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Koh, Chang-Sung (Department of Biomedical Laboratory Sciences, School of Health Sciences, Shinshu University)
Shin, Taekyun (Department of Veterinary Medicine, College of Agriculture and Life Sciences, Cheju National University)
Publication Information
Korean Journal of Veterinary Research / v.44, no.3, 2004 , pp. 349-355 More about this Journal
Abstract
The aim of this study was to evaluate the expression of galectin-3, one of beta-galactoside-binding proteins, in the experimental autoimmune encephalomyelitis(EAE) model of Lewis rats or non-obese diabetic (NOD) mice. Western blot analysis showed that galectin-3 was weakly expressed in the spinal cords of complete Freund's adjuvant(CFA) immunized control rats. In EAE, however, galectin-3 expression was significantly increased at the peak stage(days 14 post-immunization), while it was decreased slightly at the recovery stage(day 21 post-immunization). Immunohistochemical analysis showed that galectin-3 was detected in some macrophages in demyelinating lesions of NOD mice, while galectin-3 was immunoreacted in some inflammatory cells in the perivascular cuffing in rat EAE lesions. Collectively, it is postulated that the expression of galectin-3 is significantly increased in response to neuroimmunological stimulation in the central nervous system, whereas it is weak in normal rats and mice.
Keywords
galectin-3; experimental autoimmune encephalomyelitis; macrophage; animal model;
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