TGF-BETA IN AIRWAY EPITHELIAL REPAIR

TGF-β 在气道上皮修复中的作用

• 批准号: 7604761
• 负责人: STEVEN R WHITE
• 金额: $ 0.08万
• 依托单位: UNIVERSITY OF CHICAGO
• 依托单位国家: 美国
• 财政年份: 2007
• 资助国家: 美国
• 起止时间: 2007-03-01 至 2007-09-16
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7604761
• 关键词: Allergens; Apoptosis; Asthma; CDKN1A gene; Cell Cycle; Cells; Cessation of life; Computer Retrieval of Information on Scientific Projects Database; Epithelial; Epithelial Cells; Funding; Grant; Homeostasis; Inflammation; Inflammatory Response; Institution; Mediating; Process; Relative (related person); Research; Research Personnel; Resistance; Resources; Role; Source; Therapeutic Intervention; Tissues; Transforming Growth Factor beta; United States National Institutes of Health; airway epithelium; environmental agent; insight; novel therapeutics; oncoprotein p21; prevent; protective effect; receptor; repaired

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.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目和 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 气道上皮可能在对环境因素和过敏原暴露的炎症反应中受到广泛损害，部分是由于细胞凋亡。转化生长因子-β (TGF-b) 可以防止上皮细胞凋亡。鉴于 TGF-b 在介导炎症和组织重塑中的作用，了解 TGF-b 如何保护气道上皮非常重要。我们将从哮喘受试者和正常受试者中收集气道上皮，并检测 Fas 死亡受体激活后 TGF-b 保护作用的差异。我们将鉴定 Smad7、细胞周期、p21 和 p15 表达以及细胞激活方面的差异，这些差异可能解释哮喘上皮细胞对 TGF-b 保护作用的相对抵抗力。这些研究应该为控制气道上皮稳态的基本机制提供重要的新见解。了解这一过程可能会建议新的治疗干预措施，以保护气道上皮免受哮喘损伤。