MECHANISM OF SICKLE CELL RETENTION IN THE RETINAL VASCULATURE

视网膜血管中镰状细胞保留的机制

• 批准号: 6593858
• 负责人: Gerard Anthony Lutty
• 金额: $ 17.52万
• 依托单位: ALBERT EINSTEIN COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2002
• 资助国家: 美国
• 起止时间: 2002-05-20 至 2003-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6593858
• 关键词: blood vessel occlusion; cell adhesion; chronic disease /disorder; disease /disorder model; erythrocytes; genetically modified animals; hemoglobin Ss; histopathology; horseradish peroxidase; interleukin 1; laboratory mouse; laboratory rat; reticulocytes; retina circulation; retina circulation disorder; retina disorder; sickle cell anemia; tumor necrosis factor alpha

Adapted from Applicant's Abstract) PI G. Lutty will investigate the effect of the cytokines IL-1 and TNFalpha which up-regulate adhesion molecules on retention of human sickle erythrocytes in the retinal microvasculature in a rat model in which only SS4 cells (dense SS cells) are retained under normal conditions. A second hypothesis will be investigated that transgenic mice with higher levels of expression of human alpha and BetaS- globin genes have an earlier onset and more severe retinopathy and that the onset of vaso-occlusion occurs more rapidly if the animals receive LPS, which may stimulate up-regulation of adhesion molecules by mechanisms similar to those observed in the rat model.

PI G. Lutty将研究这一效应