지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
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연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학위논문
- 저자정보
- 지도교수
- 홍진태
- 발행연도
- 2016
- 저작권
- 충북대학교 논문은 저작권에 의해 보호받습니다.
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초록· 키워드
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Insulin-degrading enzyme (IDE) is a protein involved in not only the primary mechanism for insulin degradation but also a wide range of biological functions, e.g. insulin regulation, peptide clearance and transcriptional activity. Among these biological function of IDE, it also known plays important role of the enzymatic mechanism that initiates cellular insulin processing and degradation. A previous study found the IDE increased in the liver and striatum in an experimentally induced diabetic mice model. Also, both mRNA levels and expression of IDE have been reported to increase in patients with diabetes. The expression of H1/siRNAinsulin-CMV/hIDE effectively degrades the insulin secreted from the normal pancreas of a Tg mouse, and effectively induces diabetic symptoms with high blood glucose levels. Any prolonged exposure to high blood glucose levels is the key factor associated with the onset of micro-vascular diseases specific to diabetes. Hence, targeting inflammatory factors is considered a strategy to prevent and control the complications relevant to diabetes. DNA microarray is used here to identify the physiological effects of persistently high blood glucose levels due to insulin deficiency. As a result, the gene ontology analysis report demonstrates a marked increase in the expression of genes associated with inflammation, whilst the gene card report highlights the increased genetic expression related to cytokine and chemokine secretion. The present study analyzes the results of DNA microchip assay to propose a model of in inflammatory diseases ascribable to high blood glucose levels.
목차
I.Introduction 1II.Material and Methods 81. pH1/siRNAinsulin-CMV/hIDE transgenic mice 82. Blood glucose measurements 93. RNA Isolation and quality measurement 94. Target labeling and hybridization to microarray 105. Data acquisition and analysis 126. DNCB induced Ear edema 137. DNCB induced skin dermatitis 138. Histological assay 149. Statistical analysis 15III.Results 171. Image of the gene expression profile on cDNA microarray 172.Ontology categories of inflammation-regulated andimmune response-regulated gene expression 203. Genes expression levels of up-regulation and down-regulation 274. Basal glucose level measurements 295. Dinitrochlorobenzene(DNCB) induced Ear edema in The H1/siRNAinsulin-CMV/hIDE mice 316. Dinitrochlorobenzene(DNCB) induced dermatits in The H1/siRNAinsulin-CMV/hIDE mice 33IV.Discussion 36Reference 44한글초록 53Acknowledgement 55
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