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Autophagy 매개체인 LC3로 인한 Aβ 신경 독성의 증가
이승아;이현정;김도희;김옥현 박지애;김대진;정윤희;김경용;김성수;이원복 중앙대학교 의과대학 의과학연구소 2012 中央醫大誌 Vol.37 No.1/2
Autophagy is a highly regulated cellular mechanism that results in the bulk degradation process and which seems to be implicated in a variety of physiological and pathological conditions relevant to Alzheimer's disease (AD). Also, it has been suggested that the large part of autophagy is mediated by Light Chains 3 (LC3). Despite research suggesting an association between AD and autophagy, many issues remain to be addressed. To determine the relevance between autophagy and AD, we evaluated amyloid beta (Aβ) toxicity either in SH-SY5Y cells transfected with only EGFP or the cells exogeneously transfected with EGFP-LC3, mediating autophagy easily by overexpressed LC3. Without treatment of Aβ, the cell viabilities were quietly similar in both kinds of cells. The cell viability was decreased significantly in LC3 overexpressed cells. Consistently, more increased oxidative stress was detected in LC3 overexpressed cells. These results suggest that autophagy enhanced Aβ toxicity by way of increasing oxidative stress at least in part. This study will be of help to understand the role of autophagy in neurodegenerative diseases.
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