DEVELOPMENT OF AN IN VITRO WOUND HEALING MODEL

超出提供的空间。这项研究项目的长期目标是增加我们对伤口收缩过程的了解。更好地了解收缩是寻找必要的治疗策略来控制收缩和瘢痕形成的关键一步。为了达到这个目标，我们一直在研究几种不同的伤口收缩体外模型。在接下来的五年里，我们计划使用体外创伤收缩模型来研究细胞信号、收缩调节和细胞凋亡的综合方法。具体目标#1集中于由应激基质收缩、自分泌调节和即刻早期基因转录激活的丝裂原活化蛋白激酶信号转导通路。具体目标#2重点阐述了血小板衍生生长因子和溶血磷脂酸刺激应激性和漂浮性胶原收缩的机制，调节浮动和应激性基质收缩的不同，以及机械应力在肌成纤维细胞分化中的作用。具体目标#3侧重于导致经历应激基质收缩的细胞凋亡的因素。表演网站========================================Section End===========================================

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===========================================