P01-Pathogenesis and Prevention of Osteoporosis

P01-骨质疏松症的发病机制及预防

• 批准号: 6369226
• 负责人: BARBARA E KREAM
• 金额: $ 116.73万
• 依托单位: UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
• 依托单位国家: 美国
• 财政年份: 1987
• 资助国家: 美国
• 起止时间: 1987-09-30 至 2005-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6369226
• 关键词: disease /disorder prevention /control; osteoporosis; pathologic process

DESCRIPTION OF THE OVERALL PROGRAM (taken from the application): This program project application represents a coordinated, collaborative and multidisciplinary approach that utilizes common resources, facilities and instrumentation to support scientific investigators related to the pathogenesis of osteoporosis. This application is comprised of four highly integrated scientific projects and three supporting core facilities (Administration, Molecular Histology and Transgenic Animal and Molecular Cores). The central theme of the ?program project is that the pathogenesis of osteoporosis is due both to the interaction of catabolic factors that increase bone resorption and to the loss of anabolic activities. These factors, both systemic hormones and local cytokines, modulate the differentiation of osteoclast and osteoblast lineage cells and the biological function of these cells. An understanding of these factors and their actions on bone remodeling will help elucidate the pathogenesis of osteoporosis. Moreover, intervention with molecules that block pathogenic factors or enhance anabolic activities will have therapeutic implications. This could be accomplished by somatic gene therapy once the cellular and molecular steps required to develop such a strategy are developed. The scientific projects of this application are: (1) Glucocorticoids and osteoblast apoptosis, (2) Estrogen regulation of cytokine responsiveness in bone: osteoclastogenesis, (3) The roles of insulin-like growth factor and glucocorticoids on bone remodeling, and (4) Engraftment of osteoprogenitor cells in bone. We believe that interactions among our investigators, research productivity towards the central theme and new collaborations will be facilitated greatly by the program project mechanism.

总体说明（取自应用程序）：此程序 项目申请代表了一个协调，协作和 多学科方法，利用共同资源、设施和 支持与发病机制相关的科学研究者的仪器 骨质疏松症该应用程序由四个高度集成的 科学项目和三个支持核心设施（行政， 分子组织学和转基因动物和分子核心）。中央 的主题？骨质疏松症的发病机制是由于 既与增加骨吸收的分解代谢因子的相互作用有关， 合成代谢活动的丧失。这些因素，包括全身激素和 局部细胞因子，调节破骨细胞和成骨细胞的分化 谱系细胞和这些细胞的生物学功能。了解 这些因素及其对骨重建的作用将有助于阐明 骨质疏松症的发病机制。此外，用分子进行干预， 致病因素或增强合成代谢活动将有治疗 影响这可以通过体细胞基因治疗来完成， 开发了开发这种策略所需的细胞和分子步骤。 本次申请的科学项目为：（1）糖皮质激素和 成骨细胞凋亡，（2）雌激素调节细胞因子反应性， 骨：破骨细胞生成，（3）胰岛素样生长因子和 糖皮质激素对骨重建的影响;（4）骨祖细胞的移植 骨细胞我们相信，我们的调查人员之间的互动，研究 生产力对中心主题和新的合作将是 计划项目机制大大促进了这一进程。