Using CRISPR/Cas9 to Knock out Amylase in Acinar Cells Decreases Pancreatitis-Induced Autophagy

• Material Type: 博士論文
• Title: Using CRISPR/Cas9 to Knock out Amylase in Acinar Cells Decreases Pancreatitis-Induced Autophagy
• Author/Editor: 安永, 浩平
• Author Heading: 安永, 浩平
• Publication Date: 2018-09-25
• Publication Date (W3CDTF): 2018-09-25
• Alternative Title: CRISPR/Cas9を用いた腺房細胞のアミラーゼノックアウトは、膵炎により誘導されるオートファジーを減少させる。
• Contributor: 中村, 雅史; 康, 東天; 小田, 義直
• Degree grantor/type: 九州大学
• Date Granted: 2018-09-25
• Date Granted (W3CDTF): 2018-09-25
• Dissertation Number: 甲第14182号
• Degree Type: 博士（医学）
• Conferring No. (Dissertation): 甲第14182号
• Text Language Code: eng
• Target Audience: 一般
• Note (General): Pancreatic cancer is a malignant neoplasm that originates from acinar cells. Acinar cells get reprogrammed to become duct cells, resulting in pancreatic cancer. Pancreatitis is an acinar cell inflammation, leading to “impaired autophagy flux”. Pancreatitis promotes acinar-to-ductal transdifferentiation. Expression of amylase gets eliminated during the progression of pancreatic cancer. Amylase is considered as an acinar cell marker; however, its function in cells is not known.Thus, we investigated whether amylase affects the acinar cell autophagy and whether it plays any role in development of pancreatitis. Here, we knocked out ATG12 in a pancreatic cancer cells and acinar cells using CRISPR/Cas9. Autophagy inhibition led to an increase in the expression of duct cell markers and a simultaneous decrease in that of acinar cell markers. It also caused an increase in cell viability and changes in mitochondrial morphology. Next, we knocked out amylase in acinar cells. Amylase deficiency decreased autophagy induced by pancreatitis. Our results suggest that amylase controls pancreatitis-induced autophagy. We found that eliminating amylase expression contributes to pancreatic cancer etiology by decreasing autophagy. Furthermore, our results indicate that amylase plays a role in selective pancreatitis-induced autophagy of pancreatic enzyme vesicles.; PubMed番号 : 29888283
• DOI: info:doi/10.1155/2018/8719397; https://doi.org/info:doi/10.1155/2018/8719397
• Persistent ID (NDL): info:ndljp/pid/11194622; https://dl.ndl.go.jp/pid/11194622
• Collection: 障害者向け資料
• Collection (Materials For Handicapped People:1): テキストデータ
• Collection (particular): 国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文; https://dl.ndl.go.jp/collections/A00014
• Acquisition Basis: 博士論文（自動収集）
• Date Accepted (W3CDTF): 2018-12-03T16:15:19+09:00
• Date Created (W3CDTF): 2018-11-05
• Format (IMT): application/pdf
• Access Restrictions: 国立国会図書館内限定公開
• Service for the Digitized Contents Transmission Service: 図書館・個人送信対象外
• Availability of remote photoduplication service: 可
• Periodical Title (URI): http://hdl.handle.net/2324/1959085
• Data Provider (Database): 国立国会図書館 : 国立国会図書館デジタルコレクション; https://dl.ndl.go.jp

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