VEGF Expression and ER Stress in Diabetic Retinopathy

糖尿病视网膜病变中的 VEGF 表达和 ER 应激

• 批准号: 6666670
• 负责人: CHRISTOPHER N ROYBAL
• 金额: $ 2.72万
• 依托单位: UNIVERSITY OF NEW MEXICO
• 依托单位国家: 美国
• 财政年份: 2003
• 资助国家: 美国
• 起止时间: 2003-03-27 至 2005-08-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6666670
• 关键词: VEGF; Expression; ER; Stress; Diabetic

DESCRIPTION (provided by applicant): Our goal is to determine how VEGF translation and transcription is affected by ER-stress and if this mechanism plays a role in experimental retinophathy. Recent publications have shown a correlation between ER-stress and increased levels of VEGF mRNA and protein. Protein synthesis attenuation occurs during ER-stress and has prompted us to examine the role of a proposed internal ribosome entry site (IRES), located in the 5' UTR, in the translation initiation of VEGF synthesis. The role of ER-stress on angiogenesis will be further explored using an in vitro diabetic retinopathy model. The Streptozotocin (STZ) and retinopathy of prematurity (ROP) diabetic rat models are the identified models in which these studies will take place. By confirming or disproving the role of ER-stress on angiogenesis we will develop a greater understanding of vascular associated complications seen in diabetes.

描述（由申请人提供）：我们的目标是确定VEGF翻译和转录如何受到ER应激的影响，以及这种机制是否在实验性视网膜病变中起作用。最近的出版物表明ER应激与VEGF mRNA和蛋白水平升高之间存在相关性。蛋白质合成衰减发生在ER应激期间，并促使我们研究位于5' UTR中的提议的内部核糖体进入位点（IRES）在VEGF合成的翻译起始中的作用。ER应激对血管生成的作用将使用体外糖尿病视网膜病变模型进一步探索。链脲佐菌素（STZ）和早产儿视网膜病变（ROP）糖尿病大鼠模型是进行这些研究的确定模型。通过证实或反驳ER应激对血管生成的作用，我们将对糖尿病中的血管相关并发症有更深入的了解。