于福興實驗室研究計劃

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).

机标关键词：barrier function、adjuvant therapy、角膜上皮、wound healing、transcription factors、inflammatory response、inflammatory reaction、Molecular regulation、bacterial infection、therapeutic agents、corneal epithelium、consumer products、血清蛋白、protein kinase、cell migration、organ culture、cell adhesion、口愈合、分子、上皮細胞

所属期刊栏目：1

分类号：R77(眼科学)

资助基金：美国国立卫生研究院资助项目

在线出版日期：2004-01-08（万方平台首次上网日期，不代表论文的发表时间）

页数：共1页

页码：3