Keratocyte regulation in corneal repair

描述(摘自申请人的摘要)： 长期目标是确定表型的分子基础。 调节和确定角质形成细胞、成纤维细胞和肌成纤维细胞的作用 正常角膜生物学的表型以及对基质的反应 伤人。 允许研究人员复制角质形成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 肌成纤维细胞向成纤维细胞的转化将被利用。 在此应用程序中要检验的一般假设是三个 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 由三个主要因素的相互作用控制的；细胞-基质 相互作用；细胞-细胞相互作用；以及生长因子。 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作为一种基质信号影响表型、迁移和 扩散。 (3)uPA及其与跨膜蛋白相互作用对细胞的调节作用 功能。 (4)ZO-1参与成纤维细胞向肌成纤维细胞的转化。

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.