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    Please use this identifier to cite or link to this item: http://ir.lib.ncu.edu.tw/handle/987654321/84572


    Title: 綠茶表沒食子酸酯型兒茶素酸酯對脂肪細胞內微核醣核酸-143 與 -let-7a基因表現的調節之訊息傳遞路徑;Investigation of the Signal Pathways of Green Tea Epigallocatechin Gallate to Regulate Microrna-143 and Microrna-Let-7a Gene Expressions in Fat Cells
    Authors: 高永旭
    Contributors: 生命科學系
    Keywords: 綠茶;兒茶素;脂肪細胞;微核醣核酸;Green tea;catechin;fat cell;microRNA
    Date: 2020-12-08
    Issue Date: 2020-12-09 09:44:20 (UTC+8)
    Publisher: 科技部
    Abstract: 肥胖症是目前全世界(包括台灣)常見的一種疾病,與癌症、糖尿病、高血壓及心血管疾病之間相關連,主要特徵是脂肪細胞因生長與分化而使得細胞數目和內部油滴增多。而這些特徵會受到營養因子與微核醣核酸(英文簡稱miR) 所調控,《最近,我們的數據顯示在白色前脂肪細胞,綠茶表沒食子酸酯型兒茶素酸酯(英文簡稱EGCG)分別會增加24種miR基因的表現及減少26種miR基因的表現,其中正調節miR-143與miR-let-7a基因表現,也負調節兩者標的基因例如DLK1和HMGA2基因的表現。當miR-143 mimic植入白脂細胞使得miR-143大量表現時,且缺乏EGCG的處理下,除了減少DLK1基因的表現,也減少細胞數目;反之,miR-143 inhibitor植入白脂細胞後,阻擋EGCG對miR-143基因表現的正調節作用及細胞數目的減少作用。EGCG也調節棕脂和米脂細胞內miR-143與miR-let-7a基因的表現。EGCG的作用與Glutathione前驅物相似,而AMPK抑制物會阻擋EGCG對miR-143/DLK1基因表現的作用,但這些作用機轉有待釐清;此外,miR-let-7a訊息分子是否能調節EGCG對白脂細胞生長與分化的抑制作用也有待釐清;本實驗室曾發現EGCG會藉由ERK、AMPK、glutathione、EGCG受器等分子而調節脂肪細胞的功能,故假設EGCG可藉由這些分子來傳遞訊息,使得脂肪細胞miR-143和miR-let-7a基因表現受到激發,進而調節細胞生長與分化。》【為了瞭解綠茶EGCG的miR訊息路徑對肥胖症和脂肪細胞功能的影響,本三年計畫的主旨是探討它對脂肪細胞內miR-143與miR-let-7a基因表現的影響之訊息路徑,進而調節生長與分化。子目的一和二探討miR-143與miR-let-7a訊息路徑是否參與它對脂肪細胞生長與分化的抑制作用。子目的三和四探討MAPK與AMPK訊息路徑是否參與它對脂肪細胞內miR-143與miR-let-7a基因表現的影響,進而調節生長與分化。子目的五和六探討Glutathione與EGCG受器訊息路徑對它所調節脂肪細胞內miR-143與miR-let-7a基因表現的影響,進而調節生長與分化。子目的七是探討EGCG在正常小鼠和高脂食物誘導型肥胖小鼠對脂肪組織內miR-143與miR-let-7a基因表現的影響。】 ;Obesity is a common disease in the world’s population, including Taiwan, and it associates with risks of cancer, diabetes, hypertension, and cardiovascular disease. Obesity is characterized by increased number of fat cells and lipid droplet due to mitogenesis and differentiation. In turn, the two processes can be regulated by nutritional factors and microRNA (miR) molecules.《In particular, our recent preliminary data indicated that green tea epigallocatechin gallate (EGCG) upregulated 24 miR expressions and downregulated 26 miR expressions in 3T3-L1 white preadipocytes. Among them, miR-143 and miR-let-7a expressions in 3T3-L1 white preadipocytes were increased after EGCG treatment. Decreases in expressions of their respective target genes, such as DLK1 and HMGA2, induced by EGCG were also observed. When miR-143 mimics was transfected into 3T3-L1 cells in the absence of EGCG, the level of miR-143 mRNA expression was increased, the level of DLK1 gene expression was reduced, and the number of cells was decreased. Whereas, an inhibitor for miR-143 knockdown in 3T3-L1 preadipocytes antagonized EGCG-induced increase in miR-143 expression and prevented EGCG-induced decrease in cell number. EGCG also altered miR-143 and let-7a expressions in brown and brite fat cells. Interestingly, actions of EGCG on expressions of these genes were similar to those altered by a glutathione (GSH) precursor. The effects of EGCG on miR-143/DLK1 expressions were reversed by an AMPK inhibitor. However, the action mechanisms of GSH and AMPK on EGCG-mediated miR expression require further demonstrations. Whether the miR-let-7a/HMGA2-regulated pathway mediate the inhibitory effect of EGCG on the growth and differentiation of white fat cells still requires thorough demonstrations. EGCG was found by our lab to regulate fat cell functions through the ERK, AMPK, GSH, and EGCG receptor pathways; thus, the hypothesis arises that any of these signaling molecules may mediate EGCG’s actions on miR-143 and miR-let-7a genes in fat cells and thereby coordinating fat cell growth and differentiation.》【To understand the miR signaling pathway of green tea EGCG involved in its impacts on obesity and fat cell functions, the overall objective of this 3-year study is to investigate the signal pathways involved in EGCG modulations of miR-143 and miR-let-7a gene expressions in fat cells and thereby coordinating fat cell growth and differentiation. Aims I and II will study how the miR-143 and miR-let-7a signaling pathways mediate the inhibitory effects of EGCG on fat cell growth and differentiation, respectively. Aims III and IV will study if the respective MAPK and AMPK signaling pathways are involved in EGCG modulations of miR-143 and miR-let-7a gene expressions in fat cells in relation to growth and differentiation processes. Aims V and VI will study the respective GSH and EGCG receptor signaling pathways involved in EGCG modulations of miR-143 and miR-let-7a expressions in fat cells in relation to growth and differentiation processes. Aims VII will study the in vivo effects of EGCG on miR-143 and miR-let-7a levels in adipose tissues of normal and high-fat diet-induced obesity mice, respectively.】
    Relation: 財團法人國家實驗研究院科技政策研究與資訊中心
    Appears in Collections:[生命科學系] 研究計畫

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