MOLECULAR MECHANISTIC BASIS FOR RADIATION INDUCED PULMONARY LATE EFFECTS

辐射引起的肺迟发效应的分子机制基础

• 批准号: 6563658
• 负责人: Jacob N Finkelstein
• 金额: $ 15.75万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-02-01 至 2003-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6563658
• 关键词: RNase protection assay; allergic pneumonitis; alveolar macrophages; cell cell interaction; cell type; chemokine; cytokine; enzyme linked immunosorbent assay; fibroblast growth factor; gene expression; genetic strain; immunocytochemistry; in situ hybridization; ionizing radiation; laboratory mouse; medical complication; molecular pathology; neoplasm /cancer radiation therapy; protein biosynthesis; pulmonary fibrosis /granuloma; radiation dosage; radiation genetics; radiation sensitivity; respiratory epithelium; vascular endothelium

Description: (Applicant?s Description)The general goal of this program is directed at gaining a deeper understanding of the molecular mechanisms which are the basis for the normal tissue late effects which are observed in the lung following radiation. Previous CERRIS programs have led to the paradigm of radiation late effects being dependent upon the "conversation" which takes place between a number of injured cells, rather than the classic concept of a single target cell. In pursuit of this goal, they mean to further define the conversation, which they have hypothesized as a "cytokine cascade", in terms of the spatial and temporal release of proinflammatory and profibrotic cytokines and growth factors, and their genetic context. Expansion of this paradigm has led them to postulate the role of the immune system in the development of late tissue effects and this will be explored in more detail. Modulation of the cytokine cascade(s) and/or the immune system will be investigated as a means of both elucidating the roles of specific cytokines, as well as suggesting routes of amelioration.

描述：（申请人的描述）该计划的总体目标是 旨在更深入地了解其分子机制 是在正常组织中观察到的后期效应的基础 辐射后的肺。之前的 CERRIS 项目已经引领了范例 辐射后期影响取决于“对话” 放置在许多受损细胞之间，而不是经典的概念 单一靶细胞。为了实现这一目标，他们打算进一步定义 他们将其假设为“细胞因子级联”，用术语来说 促炎和促纤维化的空间和时间释放 细胞因子和生长因子及其遗传背景。扩展此 范式使他们假设免疫系统在 晚期组织效应的发展，这将被更详细地探讨。 细胞因子级联和/或免疫系统的调节将是 研究作为阐明特定细胞因子作用的一种手段， 并提出改进途径。