于福興實驗室研究計劃

• 作者: Fu-shin Yu 于福興
• 来源期刊: 美中国际眼科杂志
• 学科: 医学
• 年，卷（期）: 2001,（3）
• 所属期刊栏目: 國际学术交流
• 页码范围: 3
• 页数: 1页
• 分类号: R77
• 字数: 759字
• 语种: 中文
• DOI: 10.3969/j.issn.1672-5123.2001.03.004

摘要

1 Molecular regulation of corneal wound healing Rapid healing of the corneal epithelium in response to injury is essential for maintenance of its barrier function. The long-term goal of this project is to obtain basic information about the molecular and cell biology of corneal wound healing. The project will test the hypotheses that amyloid β/A4 precursor-like protein controls serine proteinase activity, mediates cell adhesion, and promotes cell migration during corneal reepithelialization. This study should provide the basis to begin constructing a detailed nap of the molecular pathways and interconnecting networks of proteins functioning in wound repair and to develop therapeutics for treatment of corneal diseases like recurrent erosions and persistent defects of the epithelium.2 Developing an ex vivo model for ocular irritation testThe objective of this project is to develop an ex vivo assay system to predict ocular irritation potential of test chemicals and consumer products. Our hypothesis has been that activation of these transcription factors and disruption of corneal integrity can be used as endpoints/ markers for evaluating ocular toxicity in organ culture. Our goal is to develop a sensitive, efficient, economical and reliable ex vivo model for predicting irritation potential of a chemical or consumer product with mechanistic basis.3 Modulation of epithelial barrier function during corneal infectionThe long-term goal of this project is to understand the mechanisms underlying the induction of the inflammatory reaction and breakdown of the epithelial barrier in the cornea upon infection. We will test the hypothesis that in the cornea TLRs confer responsiveness of HCE cells to pathogens, and PA challenge-induced TLR signaling, through activation of NF-?B and/ or mitogen-activated protein kinase (MAPK), contributes to infection-induced epithelial barrier breakdown. The following studies will be carried out. An understanding of how TLRs transmit signals that lead to epithelial response, including modulation of barrier function,may allow the development of therapeutic agents that prevent breakdown or enhance recovery of barrier function during infection and, as an adjuvant therapy, eliminate the corneal scarring and vision loss associated with bacterial keratitis.4 Developing an adjuvant therapy to reduce inflammatory response induced by bacterial infection of the cornea (bacterial keratitis).