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자료유형
학술저널
저자정보
김정태 (제주대학교) 안미정 (제주대학교) 최유나 (제주대학교) Poornima Ekanayake (제주대학교) 박철민 (제주대학교) 문창종 (전남대학교) 정경숙 (Immunoregulatory Materials Research Center) Akane Tanaka (Tokyo University) Hiroshi Matsuda (Tokyo University) 신태균 (제주대학교)
저널정보
한국뇌신경과학회 Experimental Neurobiology Experimental Neurobiology Vol.28 No.1
발행연도
2019.1
수록면
74 - 84 (11page)

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Olfactory dysfunction occurs in multiple sclerosis in humans, as well as in an animal model of experimental autoimmune encephalomyelitis (EAE). The aim of this study was to analyze differentially expressed genes (DEGs) in olfactory bulb of EAE-affected mice by next generation sequencing, with a particular focus on changes in olfaction-related signals. EAE was induced in C57BL/6 mice following immunization with myelin oligodendrocyte glycoprotein and adjuvant. Inflammatory lesions were identified in the olfactory bulbs as well as in the spinal cord of immunized mice. Analysis of DEGs in the olfactory bulb of EAE-affected mice revealed that 44 genes were upregulated (and which were primarily related to inflammatory mediators), while 519 genes were downregulated; among the latter, olfactory marker protein and stomatin-like 3, which have been linked to olfactory signal transduction, were significantly downregulated (log2 [fold change] >1 and p-value <0.05). These findings suggest that inflammation in the olfactory bulb of EAE-affected mice is associated with the downregulation of some olfactory signal transduction genes, particularly olfactory marker protein and stomatin-like 3, which may lead to olfactory dysfunction in an animal model of human multiple sclerosis.

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