Keratocyte regulation in corneal repair

描述（来自申请人的摘要）： 长期目标是确定表型的分子基础 调节并确定角膜基质细胞、成纤维细胞和肌成纤维细胞的贡献 表型对正常角膜生物学以及对基质的反应 伤人 一种允许研究者复制角膜细胞的模型细胞培养系统 成纤维细胞和成纤维细胞到肌成纤维细胞的转变以及逆转 将利用肌成纤维细胞到成纤维细胞的转变。 在本申请中要测试的一般假设是， 角膜基质细胞表型：角膜基质细胞、成纤维细胞和肌成纤维细胞， 细胞基质 相互作用;细胞-细胞相互作用;和生长因子。 这四个具体目标将检验以下假设： (1)矩阵产生的信号是基本的调制器， 成纤维细胞/肌成纤维细胞表型。 (2)CTGF作为基质信号影响表型、迁移和分化。 增殖 (3)uPA及其与跨膜蛋白的相互作用调节细胞凋亡 功能 (4)ZO-1参与成纤维细胞向肌成纤维细胞的转变。

DESCRIPTION (From the Applicant's Abstract): The long-term objectives are to determine the molecular basis of phenotype regulation and define the contributions of the keratocyte, fibroblast and myofibroblast phenotypes to normal corneal biology as well as the response to stromal wounding. A model cell culture system allowing the investigator to reproduce keratocyte to fibroblast and fibroblast to myofibroblast transitions as well as reverse the myofibroblast to fibroblast transition will be utilized. The general hypothesis to be tested in this application is that the three corneal stromal cell phenotypes: keratocyte, fibroblast and myofibroblast are controlled by the interaction of three dominant factors; cell-matrix interactions; cell-cell interactions; and growth factors. The four specific aims will test the hypotheses that: (1) matrix generated signals are essential modulators of the fibroblast/myofibroblast phenotypes. (2) CTGF acts as a matrix signal to influence phenotype, migration and proliferation. (3) uPA and its interaction with transmembrane proteins modulates cellular function. (4) ZO-1 is involved in the fibroblast to myofibroblast transition.