DEVELOPMENT OF AN IN VITRO WOUND HEALING MODEL

超出所提供的空间。这个研究项目的长期目标是增加我们对伤口收缩过程的理解。在寻找控制收缩和瘢痕形成所需的治疗策略时，更好地理解收缩是必不可少的一步。为了实现这一目标，我们一直在研究几种体外伤口收缩模型的变体。在接下来的五年里，我们计划采用一种综合的方法，我们将使用体外伤口收缩模型来研究细胞信号传导、收缩调节和凋亡。Specific Aim #1聚焦于有丝分裂原激活的蛋白激酶信号转导途径，由应激基质收缩、自分泌调节和即时早期基因转录激活。特异性目标#2侧重于血小板衍生生长因子和溶血磷脂酸刺激应激和漂浮胶原收缩的机制，漂浮和应激基质收缩调节的差异，以及机械应力在肌成纤维细胞分化中的作用。特异性目标#3侧重于促进细胞凋亡的因素经历应激基质收缩。网站性能 ======================================== 节结束 ===========================================

EXCEED THE SPACE PROVIDED. The long term goal of this research project is to increase our understanding of the wound contraction process. A better understanding of contraction is an essential step in the search for therapeutic strategies necessary to control contraction and scarring. Towards this goal, we have been studying several variations of an in vitro model of wound contraction. During the next five years, we plan an integrated approach in which we will use the in vitro wound contraction model to study cell signaling, regulation of contraction, and apoptosis. Specific Aim #1 focuses on the mitogen-activated protein kinase signal transduction pathways activated by stressed matrix contraction, autocrine regulation, and immediate early gene transcription. Specific Aim #2 focuses on the mechanisms responsible for stimulation of stressed and floating collagen contraction by platelet-derived growth factor and lysophosphatidic acid, differences in the regulation of floating and stressed matrix contraction, and the role of mechanical stress in myofibroblast differentiation. Specific Aim #3 focuses on the factors that contribute to apoptosis of cells undergoing stressed matrix contraction. PERFORMANCE SITE ========================================Section End===========================================