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: 6646652
• 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/6646652
• 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.

改编自申请人的摘要）Pi G. Lutty将调查效果 细胞因子IL-1和TNFALPHA上调粘附分子在 在视网膜微脉管系统中保留人类镰状红细胞 仅保留在 正常情况。将研究第二个假设 人α和β-具有较高表达水平的转基因小鼠 Globin基因患有更早的发病和更严重的视网膜病，并且 如果动物接受的话，血管咬合的发作会更快地发生 LPS，可以通过机制刺激粘附分子的上调 与大鼠模型中观察到的类似。