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Identification of novel genes associated with progression of non-alcoholic fatty liver disease(NAFLD)

Other Titles
 비 알코올성 지방간 질환에 관련된 새로운 유전자 발굴 및 기능 분석 
Authors
 한지윤 
Degree
석사
Issue Date
2018
Description
의과학
Abstract
Non-alcoholic fatty liver disease (NAFLD) is one of the most common causes of chronic liver disease worldwide. NAFLD has become an issue contributed to the fact that it can progress towards a more severe form of the disease, the non-alcoholic steatohepatitis (NASH), which can further progress towards liver cirrhosis and even cancer. However, there is currently no approved treatment for NAFLD due to the fact that NAFLD models mimicking either steatosis or NASH-Fibrosis have been sporadically known in in vitro and in vivo, respectively. So there have limitations in studying the progression of liver disease progression from steatosis to NASH-Fibrosis. Therefore, in many countries, people are currently conducting research with significant interest in the development and validation of cell and mouse models for NAFLD. In this study, I found the most appropriate model among the various liver disease models previously reported. Using this model, I assessed the suitability through validation with gene markers that are mainly expressed in steatosis or NASH-Fibrosis. Based on the previous study, oleic acids (OA) and high fat diets (HFD) were used to make model to induce steatosis in cell (Hepa1-6, primary hepatocytes) and mouse, respectively. Also, the TGFβ with FFA mixture (OA and PA) and the choline-deficient, L-amino acid-defined, high-fat diets (CDAHFD) were used to induce the NASH-Fibrosis model in cell (LX-2, hepatic stellate cells) and mouse, respectively. Ultimately, a final goal was to add a human data in addition to established cell and mouse models because it is the major purpose of this study, which is to apply to human patients suffering from liver diseases including NAFLD. Taken together, the aim of this study is to find an unknown gene which is commonly increased in fatty liver and NASH-Fibrosis stage compared with normal liver by using integrated models (cell, mouse, and human) newly developed. By analyzing established in vitro and in vivo models with Quant-seq, it is available to find novel genes increased in NAFLD groups compared to control groups, such as ITGAX, STC1. Also, these results provide an opportunity to determine which liver disease stage belongs to the overall NAFLD spectrum with gene expression.
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Appears in Collections:
1. College of Medicine (의과대학) > Others (기타) > 2. Thesis
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/166385
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