Investigation of immune tolerance in the islet transplantation using adipose tissue derived stem cell.

使用脂肪组织来源的干细胞研究胰岛移植中的免疫耐受性。

• 批准号: 23592010
• 负责人: IWATA Takashi
• 金额: $ 3.24万
• 依托单位: The University of Tokushima
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Scientific Research (C)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2013
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23592010/
• 关键词: 膵島移植; 拒絶反応; 脂肪由来幹細胞; 免疫寛容; trophic効果; homing効果; OP9DL1細胞; VEGF signal; 脂肪由来幹細胞（ADSC）; 調節性T細胞 Treg; helper T細胞; suppressor T細胞

Cocultivation OP9-DL1 cell and human ADSC was performed, but pollution in culture enforced to take time. As an allied experiment, the cocultivation ADSC with the pancreatic islet, ADSC with hepatocytes, and the liver segmental resection+I/R+ ADSC, STZ injured pancreas+ADSC model were performed. Trophic effect and homing effect were investigated in remnant liver and injured pancreas.Cocultivation: cell viability was high in both groups, and VEGF density was high prices out of the culture fluid in both groups. When anti VEGF antibody was added in culture fluid, pancreatic islet viabilty decreased. Thus it was thought that VEGF signal might be key signal of the pancreatic islet protection. In the liver segmental resection+I/R+ADSC model, ADSC showed homing in remnant liver. The hepatocytes with SDF-1appearance changed into non-substance cell. There was no homing of ADSC in STZ injured pancreas + ADSC model.ADSC showed organ-specifically trophic, homing, and a cell protection effect.

OP9-DL1细胞和人ADSC共培养，但培养过程中的污染是需要时间的。作为联合实验，采用ADSC与胰岛共培养、ADSC与肝细胞共培养、肝段切除+I/R+ADSC、STZ损伤胰腺+ADSC模型。共培养：两组细胞存活率均较高，培养液中的血管内皮生长因子浓度较高。当培养液中加入抗血管内皮生长因子抗体时，胰岛活力下降。因此，认为血管内皮生长因子信号可能是胰岛保护的关键信号。在肝段切除+I/R+ADSC模型中，ADSC在残肝内呈归巢状态。出现SDF-1的肝细胞变为非物质细胞。在STZ损伤的胰腺+ADSC模型中，ADSC没有归巢，ADSC具有器官特异性的营养、归巢和细胞保护作用。

项目成果

Characteristics of internal hernia after gastrectomy with Roux-en-Y reconstruction for gastric cancer

• DOI: 10.1007/s00464-013-3384-7
• 发表时间: 2014-06-01
• 期刊: SURGICAL ENDOSCOPY AND OTHER INTERVENTIONAL TECHNIQUES
• 影响因子: 3.1
• 作者: Yoshikawa, Kozo;Shimada, Mitsuo;Eto, Syohei
• 通讯作者: Eto, Syohei