The inhibitory role of incretin mimetics against lung injury-induced by Toll-like receptor-mediated signaling.

肠促胰素模拟物对 Toll 样受体介导的信号传导诱导的肺损伤的抑制作用。

• 批准号: 23790924
• 负责人: NUMATA Takanori
• 金额: $ 2.16万
• 依托单位: Jikei University School of Medicine
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2011
• 资助国家: 日本
• 起止时间: 2011 至 2012
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-23790924/
• 关键词: 肺線維症; 肺傷害; インクレチン

Glucagon-like peptide-1 (GLP-1) and gastric inhibitory peptide(GIP) are known incretin hormones. To elucidate the potential role of incretins in prevention of lung injury, we analyzed the expression of incretin receptors and effect of exendin-4, a GLP-1 receptor agonist. Although neither expression of incretin receptors nor effect of exendin-4 was demonstrated in cell culturing models, type II pneumocytes in lung tissue expressed GLP-1 receptor. GLP-1 receptor expression in type II pneumocyte was especially increased in idiopathic pulmonary fibrosis (IPF), suggesting the potential involvement of incretin in IPF pathogenesis.

胰高血糖素样肽-1 （GLP-1）和胃抑制肽（GIP）是已知的肠促胰岛素激素。为了阐明肠促胰岛素在预防肺损伤中的潜在作用，我们分析了肠促胰岛素受体的表达和exendin-4（一种GLP-1受体激动剂）的作用。虽然在细胞培养模型中既没有肠促胰岛素受体的表达，也没有exendin-4的作用，但肺组织中的II型肺细胞表达GLP-1受体。II型肺细胞中GLP-1受体的表达在特发性肺纤维化（IPF）中尤其升高，提示肠促胰岛素可能参与IPF的发病机制。

项目成果

Apoptosis inhibitor of macrophage (AIM) expression in alveolar macrophages in COPD.

• DOI: 10.1186/1465-9921-14-30
• 发表时间: 2013-03-05
• 期刊: Respiratory research
• 影响因子: 5.8
• 作者: Kojima J;Araya J;Hara H;Ito S;Takasaka N;Kobayashi K;Fujii S;Tsurushige C;Numata T;Ishikawa T;Shimizu K;Kawaishi M;Saito K;Kamiya N;Hirano J;Odaka M;Morikawa T;Hano H;Arai S;Miyazaki T;Kaneko Y;Nakayama K;Kuwano K
• 通讯作者: Kuwano K

Insufficient autophagy promotes bronchial epithelial cell senescence in chronic obstructive pulmonary disease.

• DOI: 10.4161/onci.20297
• 发表时间: 2012-08-01
• 期刊: Oncoimmunology
• 影响因子: 7.2
• 作者: Fujii S;Hara H;Araya J;Takasaka N;Kojima J;Ito S;Minagawa S;Yumino Y;Ishikawa T;Numata T;Kawaishi M;Hirano J;Odaka M;Morikawa T;Nishimura S;Nakayama K;Kuwano K
• 通讯作者: Kuwano K