Impaired tissue contraction in would healing promotes development of Barrett's esophgaus

• Project/Area Number: 15K08945
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Gastroenterology
• Research Institution: Tohoku University
• Principal Investigator: Kiyotaka Asanuma 東北大学, 医学系研究科, 助教 (10431553)
• Co-Investigator(Kenkyū-buntansha): 飯島 克則 秋田大学, 医学(系)研究科(研究院), 教授 (60375003)
• Research Collaborator: FUJIYA Taku 東北大学, 大学院医学系研究科・消化器病態学分野
• Project Period (FY): 2015-04-01 – 2018-03-31
• Project Status: Completed (Fiscal Year 2017)
• Budget Amount: ¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000); Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000); Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000); Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
• Keywords: Barrett's esophagus / Nitric oxide / Wound contraction / RhoA / fibroblast / GERD / 一酸化窒素 / バレット食道 / 創傷治癒 / 組織収縮 / びらん性食道炎 / 線維芽細胞

Outline of Final Research Achievements

Barrett's Esophagus (BE) develops in the process that esophageal epithelium damaged by acid reflux heals. We have reported that development of BE is promoted by high levels of nitric oxide (NO) which arise in esophageal lumen by chemical reaction between acidified gastric juice and salivary nitrite. In the current study using immortalized human esophageal fibroblasts, we revealed that NO reduced tissue contraction ability in wound healing. Moreover, NO inhibited differentiation of myofibroblasts by decreasing expression in a-SMA in the cells. These findings suggest that impaired epithelial wound healing in esophagus could contribute to the development of BE, which is primary risk factor of esophageal adenocarcinoma.