TGF-BETA IN AIRWAY EPITHELIAL REPAIR

TGF-β 在气道上皮修复中的作用

• 批准号: 7378628
• 负责人: STEVEN R WHITE
• 金额: $ 0.14万
• 依托单位: UNIVERSITY OF CHICAGO
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-18 至 2007-02-28
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7378628
• 关键词: apoptosis; epithelium

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. The airway epithelium may be damaged extensively in inflammatory responses to environmental agents and allergen exposure, in part by apoptosis. Transforming growth factor-beta (TGF-b) may prevent epithelial cell apoptosis. Given the role of TGF-b in mediating both inflammation and tissue remodeling, Understanding how TGF-b protects airway epithelium is of importance. We will grow airway epithelium collected from asthmatic and normal subjects and examine differences in the protective effect of TGF-b after activation of the Fas death receptor. We will identify differences in Smad7, cell cycle, p21 and p15 expression, and cell activation that may explain the relative resistance of asthmatic epithelial cells to the protective effect of TGF-b. These studies should provide important new insights into a fundamental mechanism controlling airway epithelial homeostasis. Understanding the process may suggest new therapeutic interventions to protect the airway epithelium form damage in asthma.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。子弹和调查员（PI）可能已经从其他NIH来源获得了主要资金，因此可以在其他清晰的条目中代表。列出的机构适用于该中心，这不一定是调查员的机构。气道上皮在对环境药物和过敏原暴露的炎症反应中可能会受到广泛损害，部分原因是凋亡。转化生长因子β（TGF-B）可能会预防上皮细胞凋亡。鉴于TGF-B在介导炎症和组织重塑中的作用，了解TGF-B如何保护气道上皮是重要的。我们将种植从哮喘和正常受试者中收集的气道上皮，并检查FAS死亡受体激活后TGF-B保护作用的差异。我们将确定SMAD7，细胞周期，P21和P15表达的差异以及细胞活化，这些差异可能解释了哮喘上皮细胞对TGF-B的保护作用的相对抗性。这些研究应为控制气道上皮稳态的基本机制提供重要的新见解。了解该过程可能会提出新的治疗干预措施，以保护哮喘中的气道上皮损害。