EGFR-MEDIATED CORNEAL EPITHELIAL WOUND HEALING

EGFR 介导的角膜上皮伤口愈合

• 批准号: 8168354
• 负责人: BRIAN P. CERESA
• 金额: $ 21.89万
• 依托单位: UNIVERSITY OF OKLAHOMA HLTH SCIENCES CTR
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-07-01 至 2011-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8168354
• 关键词: Area; Blocking Antibodies; Computer Retrieval of Information on Scientific Projects Database; Cornea; Corneal Injury; EGF gene; Epidermal Growth Factor Receptor; Epithelial Cells; Funding; Grant; Homeostasis; Impaired wound healing; Institution; Ligands; Mediating; Molecular; Process; Research; Research Personnel; Resources; Signal Transduction; Source; Stratification; Testing; Therapeutic; United States National Institutes of Health; Wound Healing; cell motility; corneal epithelium; inhibitor/antagonist; small molecule

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Corneal epithelial wound healing and homeostasis is regulated by EGFR activity. This process is mediated by three cellular changes: cell migration, proliferation, and stratification. Inhibition of ligand-stimulated EGFR activation, either through small molecule inhibitors or blocking antibodies, results in a decrease in all three cellular changes as well as impaired wound healing. Despite evidence that the EGFR is necessary and sufficient for corneal epithelial homeostasis and wound healing, EGF has limited therapeutic utility. We hypothesize that corneal wound healing can be enhanced by promoting EGFR-mediated signals that enhance cell migration. To test this hypothesis, we must understand EGFR-mediated signaling on the molecular and cellular level. This information will be used to target molecules and mechanisms that promote epithelial cell migration, which can ultimately accelerate coverage of the damaged area and healing of the wounded cornea.

该子项目是利用该技术的众多研究子项目之一 资源由 NIH/NCRR 资助的中心拨款提供。子项目及 研究者 (PI) 可能已从 NIH 的另一个来源获得主要资金， 因此可以在其他 CRISP 条目中表示。列出的机构是 对于中心来说，它不一定是研究者的机构。 角膜上皮伤口愈合和体内平衡受 EGFR 活性调节。 该过程由三种细胞变化介导：细胞迁移、增殖和分层。通过小分子抑制剂或阻断抗体抑制配体刺激的 EGFR 激活，会导致所有三种细胞变化减少以及伤口愈合受损。尽管有证据表明 EGFR 对于角膜上皮稳态和伤口愈合是必要且充分的，但 EGF 的治疗效用有限。 我们假设可以通过促进 EGFR 介导的信号增强细胞迁移来增强角膜伤口愈合。为了检验这一假设，我们必须在分子和细胞水平上了解 EGFR 介导的信号传导。这些信息将用于靶向促进上皮细胞迁移的分子和机制，最终可以加速受损区域的覆盖和受伤角膜的愈合。